awad hashim bakheit omer - connecting …awad hashim bakheit omer khartoum, june 2009 abstract 15 in...

Evaluation of some intravenous

anaesthetic protocols for use in Female

Desert Goats in Sudan

By

Awad Hashim Bakheit Omer

B. V. Sc. (2002) University of Nyala

Supervisor

Dr. Abbas Taha Hamza Sobair

(B. V. Sc.; Ph.D.)

A thesis submitted to the Graduate College University of Khartoum in partial

fulfillment of the requirements of Master degree in Veterinary medicine in the

Department of Surgery and anaesthesia, Faculty of Veterinary Medicine.

September, 2010

2

Dedication

To the ideal specimen of the straight forwards, honest, sincere, diligent,

perseverant

To my Father and Mother

To Dr. Ajab ahmed al Ajab, and his wife

To the soul of Atta Talab

To my sisters, brothers, uncles, aunts and friends


3

TABLE OF CONTENTS

Table of contents …………………...……..….……………….………………. I

List of tables …………….………………..…………..….……………………. V

List of figures ……………….…………………..…….…….…...…............... VII

List of abbreviations ……….………………………………………..……….. IX

Acknowledgements ………..…...………………….…………………………. X

English Abstract ……………………..…...………………….……................ XII

CHAPTER ONE

INTRODUCTION & LITERATURE REVIEW

Introduction………… ……………………………………………….………… 1

1 Intravenous anaesthesia ……………..…………………….………... 4

1.1 Thiopentone sodium (thiopental)………………………………… 5

1.1.1 Identity…………………………….…………………..…………… 5

1.1.2 Chemical name…………………………….……………….……… 5

1.1.3 Molecular formula……………………………….………………… 5

1.1.4 Mode of action………………………….…………………………… 5

1.1.5 Pharmacology…………………………..……………………………. 7

1.1.6 Toxic effects………………………….……………………………… 8

1.1.7 Use of Thiopentone sodium in goats………………………………... 9

1.2 Ketamine Hcl (Ketalar)………..……………………...…………… 9

1.2.1 Identity…………………………….………………………………… 10

1.2.2 Chemical name…………………………..………………………… 10

1.2.3 Molecular formula………………………….……………………… 10

1.2.4 Mode of action……………………………………………...……… 10

1.2.5 Pharmacology………………………………………………...…….. 10

1.2.6 Toxic effects………………………………………………………… 12

4

1.2.7 Use of Ketamine Hcl in goats…………………………….………... 12

1.3 Diazepam …………………………………………………………… 12

1.3.1 Identity…………….…...………………………………...………… 13

1.3.2 Chemical name……………………..…………….………………… 13

1.3.3 Molecular formula………………….……………………………… 13

1.3.4 Mode of action…………………….………..……………...……… 15

1.3.5 Pharmacology…………………...…………..………………...…….. 15

1.3.6 Toxic effects………………………………………………………… 15

1.3.7 Use of Diazepam in goats………..……….……………..….………... 15

1.4 Xylazine……………………………………...……………….…… 16

1.4.1 Identity………………………...………….……………...………… 16

1.4.2 Chemical name…………………….…………….………….……… 16

1.4.3 Molecular formula………………………………………….……… 16

1.4.4 Mode of action……………………………..…………….....……… 18

1.4.5 Pharmacology…………………..…………..………………...…..….. 18

1.4.6 Toxic effects……………………………………………………..… 19

1.4.7 Use of Xylazine in goats………………………………………….... 20

1.5 Medetomidine ……………..……………………...……………… 20

1.5.1 Identity……………………………...………….……………...…… 21

1.5.2 Chemical name………………………….…………….…………… 21

38 Molecular formula……………………….………………………… 21

39 Mode of action…………………………………..……….....……… 21

40 Pharmacology……………………….…………..…………...…….. 23

41 Toxic effects………………………………………………..…..…… 24

42 Use of Medetomidine in goats……….….…………..….…...……... 24

CHAPTER TWO

5

MATERIALS & METHODS

2.1 Place of study ………………………………….…………………… 26

2.2 Experimental animals ……………………………………………… 26

2.3 Drugs ……………………………………………………………….. 26

2.4 Injection set ………………………………………………………… 26

2.5 Monitoring tools …………………………………………………….. 31

2.6 Anaesthetic protocols ……………………………………………… 31

2.7 Experimental design……………………………………………….. 31

2.7.1 First experiment…………………………………………………….. 32

2.7.2 Second experiment………………………………………………….. 32

2.7.3 Third experiment…………………………………………….............. 32

2.7.4 Fourth experiment…………………………………………............. 32

2.7.5 Fifth experiment………………………………………………........... 32

2.7.6 Sixth experiment……………………………………………….......... 32

2.7.7 Seventh experiment…………………………………………............. 33

2.7.8 Eighth experiment....………………………………………………... 33

2.8 Physiological parameters…………………………………..……… 33

2.8.1 Respiratory rate…………………………………………………….. 33

2.8.2 Heart rate…………………………………………………………… 33

2.8.3 Rectal temperature………………………………………………….. 33

2.9 Phases of anaesthesia …………………………………...………… 34

2.9.1 Induction phase ……………………………………………………. 34

2.9.2 Anaesthetic phase …………………………………………………. 34

2.9.3 Basal narcosis ……………………………………………………… 34

2.9.4 Lateral recumbancy ……………………………………….............. 34

2.9.5 Sternal recumbancy …………………………………………............. 34

6

2.9.6 Standing phase …………………………………………………….. 34

2.9.7 Recovery ……………………………………………………………. 35

2.9.8 Total recovery ……………………………………………………… 35

2.10 Reflexes …………………………………………………………….. 35

2.10.1 Tongue …………………………………………………….............. 35

2.10.2 Palpepral …………………………………………………………… 35

2.10.3 Swallowing …………………………………………………………. 35

2.10.4 Pedal ……………………………………………………….............. 35

2.10.5 Jaw relaxation reflex………………………………………............... 36

2.10.6 Anal ………………………………………………………………… 36

2.10.7 Cough ……………………………………………………………… 36

2.11 Statistical analysis ………………………………………………… 36

CHAPTER THREE

RESULTS

3.1 Effects of different anaesthetic protocols on the respiratory rate, heart

rate and rectal temperature …………………………………….

37

3.2 Duration of different anaesthetic phases following induction of

anaesthesia with different protocols ………………………………....

55

3.3 Signs observed following injection of selected premedications…….. 56

3.4 Signs observed following injection of selected anaesthetics ……….. 56

3.5 Signs observed due to injection of different selected combination

protocols ……………………………………………………………

57

3.6 Effect of different selected anaesthetic protocols on reflexes ………. 57

3.7 Occurrence of apnoea and regaining of spontaneous respiration due to

thiopental ………………………………………………………….

58

CHAPTER FOUR

7

DISCUSSION

4 Discussion …………………………………………………………. 67

CONCLUSION AND RECOMMENDATIONS

5.1 Conclusion………..………..………………………………………. 77

5.2 Recommendations…….……………………………………..…….. 77

References ………………………………..………..………….………….….. 78

Arabic abstract ...…………………………..……..………….………….……. 91

8

LIST OF TABLES

No. Table Page

1 Effects of Ketamine Hcl on physiological parameters (respiratory rate,

heart rate and rectal temperature) during the course of anaesthesia…...

38

2 Effect of protocol KT-DI on physiological parameters (respiratory rate,

heart rate and rectal temperature) during the course of

anaesthesia…………………………………………………………….

39

3 Effect of protocol KT-XY on physiological parameters (respiratory rate,

heart rate and rectal temperature) during the course of anaesthesia

……………………………………………………………

40

4 Effect of protocol KT-ME on physiological parameters (respiratory rate,


……………………………………………………………

41

5 Effect of Thiopentone sodium on physiological parameters (respiratory

rate, heart rate and rectal temperature) during the course of anaesthesia

…………………………………………………………

47

6 Effects of protocol TH-DI on physiological parameters (respiratory rate,


……………………………………………………………

48

7 Effects of protocol TH-XY on physiological parameters (respiratory rate,


……………………………………………………………

49

8 Effects of protocol TH-ME on physiological parameters (respiratory rate,


……………………………………………………………

50

9 Duration of different anaesthetic phases after induction of anaesthesia

9

with different selected protocols ………………................................ 59

10 Effects of different selected anaesthetic protocols on selected reflexes 61

11 Duration of Total recovery time (TRT) …………..………………... 63

12 Occurrence of apnea and regaining time of spontaneous respiration

associated with protocols containing thiopental…………………….

65

10

LIST OF FIGURES

No. Figure Page

1.1 Chemical structure of Thiopentone sodium….………………… 6

1.2 Chemical structure of Ketamine Hcl …………..……………… 11

1.3 Chemical structure of Diazepam …………………….………... 14

1.4 Chemical structure of Xylazine …………………………..…… 17

1.5 Chemical structure of Medetomidine …………………………. 22

2.1 Pre-anaesthetic medications used in different protocols……… 27

2.2 The intravenous anaesthetic drugs used in the different protocols

……………………………………………………….

28

2.3 Syringes with different size levels used in performing anaesthetic

protocols …………………………………………..

29

2.4 Monitoring tools used for monitoring physiological parameters

tested……………………………………………………………

30

3.1 Effects of Ketamine Hcl on physiological parameters (respiratory

rate, heart rate and rectal temperature) during the course of

anaesthesia …………………………..……………..

42

3.2 Effects of protocol KT-DI on physiological parameters

(respiratory rate, heart rate and rectal temperature) during the

course of anaesthesia ……………………………………..….

43

3.3 Effect of protocol KT-XY on physiological parameters


course of anaesthesia ………………………………….………

44

3.4 Effect of protocol KT-ME on physiological parameters


11

course of anaesthesia ………………………………………… 45

3.5 Effect of Thiopentone sodium on physiological parameters


course of anaesthesia ………………………..………………

51

3.6

Effects of protocol TH-DI on physiological parameters



52

3.7

Effects of protocol TH-XY on physiological parameters


course of anaesthesia …………………………………………

53

3.8

Effects of protocol TH-ME on physiological parameters



54

3.9 Duration of different anaesthetic phases after induction of

anaesthesia with different selected protocols …………..……..

60

3.10 Comparison between the different reflexes tested following

application of the different anaesthetic protocols……………..

62

3.11 Comparison of Total recovery time (TRT) duration in the different

anaesthetic protocols…….. ……………………….

64

3.12 Occurrence of apnea and regaining time of spontaneous

respiration associated with protocols containing thiopental…….

66

12

LIST OF ABBREVIATIONS

KT Ketamine Hcl at dose rate 4 mg/kg (Without premedication).

KT- DI Diazepam 0.5 mg/kg + Ketamine Hcl at dose rate 4 mg/kg

KT- XY Xylazine (2%) 0.1 mg/kg + Ketamine Hcl 4 mg/kg

KT-ME Medetomidine 10 µg/kg + Ketamine Hcl 4 mg/kg

TH Thiopentone sodium 2.5% at dose rate 10mg/kg (Without

premedication).

TH-DI Diazepam 0.5 mg/kg + Thiopentone sodium 2.5% at dose rate 10

mg/kg

TH-XY Xylazine (2%) 0.1 mg/kg + Thiopentone sodium 2.5% at dose rate

10 mg/kg

TH-ME Medetomidine 10 µg/kg + Thiopentone sodium 2.5% at dose rate

10 mg/kg

TRT Total recovery time

13

ACKNOWLEDGEMENTS

I would like to express my deepest gratitude and sincere appreciation to my

supervisor Dr. Abbas Taha Hamza Sobair, Department of Surgery and anaesthesia,

Faculty of Veterinary Medicine, University of Khartoum, for his unfailing

guidance, constructive criticism, encouragement and for the considerable assistance

throughout this work.

The keen interest of the staff of the Department of Clinical studies especially

Dr. Mohammed Ahmed Hassan Ghurashi, Dr. Hisham Ismail Seri Farah and Dr.

Abd elmutalab Ali Elmubark who offered every possible assistance required to

make this study possible, is highly acknowledged. This study would have been

difficult to complete without their support. Duel thanks are extended to my

colleagues in the Faculty of Veterinary Science, University of Nyala for the help

during the experimental part of the study, and to technicians Ahmed Adam

Mohamed Alam Eldin, Ahmed Ibrahim Osman, Abd elraheem Abd elrahman,

Mohammed Suleiman, and Aziza Hassan for their valuable help and

encouragement during this study.

The logistic support to the experimental part was kindly provided through

our senior technician Mr. Mohamed Karm Eldin Arfa, he is always there providing

his help and support.

This study was made possible through a scholarship provided to me by

University of Nyala, in this contest I would like to express my appreciation to Prof.

Adam Dawoud Abakar the former academic secretary and to Dr. Abakar Adam

Mohamed the present academic secretary, and Dr. Ahmmed Alhaj Bashar the dean

faculty.

Special thanks to Dr. Alwasila Mokhtar Mohammed for his help with the

statistical analysis of data in this study.

14

My thanks are also extended to Dr. Nasr Eldein Eltaib, Dr. Borhan Nasur,

Dr. Modather Al taib, Dr. Sarah Mohammed, Dr Siham Adam, Siham Mahmood,

Dr. Ahmed Ali, Dr. Osama Essa, Yasir H Almahi, Dr. Mobark H. Bilal, Ali Abbas

Ajab, Jalal, Ahmed, Emmad, Osman, Nabaro, Sardia for their encouragement and

support.

Above all, praise is to Allah, the Compassionate, and the most Merciful for

giving me the health and strength to carry out this work.


Khartoum, June 2009

Abstract

15

In this study, it is decided to throw light on some intravenous anaesthetic

protocols to be used in female desert goats in Sudan. The main objective of this

study is to provide baseline data pertaining to different anaesthetic phases tested

and to compare and contrast the different examined protocols.

This study was conducted using 64 healthy female desert goats divided

randomly into eight groups of equal size. Ketamine Hcl (KT) (5%) at dose rate of

4mg/kg body weight and Thiopentone Sodium (TH) (2.5%) at dose rate of 10mg/kg

body weight were used as induction agents injected intravenously in all examined

protocols. Diazepam (DI) (0.5%) at dose rate of 0.5mg/kg body weight, Xylazine

(XY) (2%) at dose rate of 0.1mg/kg body weight and Medetomidine (ME) at dose

rate of 10µg/kg body weight were used as premedications, individually injected

intravenously 10 minutes prior to Ketamine Hcl or Thiopentone Sodium (TH)

injection. Each of the above mentioned groups of animals were subjected to

treatment either with KT or TH with or without one of the above mentioned

premedications, so the tested protocols were KT, KT-DI, KT-XY, KT-ME, TH,

TH-DI, TH-XY and TH-ME.

Respiratory rate, heart rate and rectal temperature were measured before and

immediately after injection of premedications and anaesthetics at 10 minutes

intervals until full recovery was attained as monitor, using standard clinical

methods. The major reflexes were monitored throughout the course of anaesthesia.

The usage of the protocols KT, KT-XY and KT-ME induced significant

increase in respiratory rate, while TH-DI and TH-XY exerted significant decrease

in respiration. There was significant tachycardia due to injection of TH, TH-DI and

TH-XY, and significant bradycardia due to injection of TH-ME. The usage of TH

and TH-DI induced significant hyperthermia, while none of the protocols tested

harboured significant hypothermia.

16

Thiopentone sodium containing protocols (TH-DI, TH-XY, and TH-ME)

were found to have longer duration of anaesthetic phase, when compared with that

observed with Ketamine or Thiopentone sodium when used without premedication.

The longest duration of basal narcosis was induced with the protocol TH-ME,

while KT harboured the shortest one. The protocol KT-ME induced the longest

mean period of lateral recumbancy phase and KT-DI exerted the shortest one. The

longest mean value of the sternal recumbancy phase in different protocols tested

was induced with TH-DI, while the KT-XY harboured the shortest one. The longest

mean value of standing phase was noticed with TH-DI, and the shortest one with

ME-KT. There was no obvious relationship between phases of anaesthesia and

regained time of selected reflexes tested.

There is significant increase in total recovery time (TRT) when

premedications were used prior to Ketamine or Thiopentone sodium. Also

generally, Thiopentone sodium containing protocols were reported to have

significantly longer duration of TRT than Ketamine Hcl containing protocols.

Apnoea was observed when Thiopentone sodium containing protocols were

used. The longest duration of apnoea was induced with TH-DI, the shortest one was

due to injection of TH-XY.

This study concludes that each of the eight tested protocols at the prescribed

dose rates is safe for use in female desert goats, with variable effects on

physiological and anaesthetic parameters.

17

INTRODUCTION

Introduction

18

Goats seem to have been first domesticated roughly 10,000 years ago in the

Zagros Mountains of Iran. The domestic goat (Capra aegagrus hircus) is a

domesticated subspecies of the wild goat of southwest Asia and Eastern Europe. It is a

member of the bovine family and is closely related to the sheep, both being in the

goat antelope group. They have been used for their milk, meat, hair, and skins all over

the world. In the last century they have also gained some popularity as pets.

Historically, goat hide has been used for water and wine bottles in both traveling

and transporting wine for sale. It has also been used to produce parchment, which

was the most common material used for writing in Europe until the invention of the

printing press. Goats are gaining acceptance as an established model for biomedical

research and for surgical training and teaching. They are used in medical,

orthopedic, psychological, chemotherapeutic, and physiologic research (Lincicome

and Hall, 1984).

General anaesthesia either it is intravenous or inhalation anaesthesia is

increasingly being used for surgical interferences in goats, such as caesarean

section embryotransfere, laparotomy, and the various amputations.

Anaesthesia is required whenever an animal is subjected to surgery. It’s vital

from humanitarian point of view, but it is also required by law that effective

measures are adopted to prevent suffering during painful procedures. There are also

times when anaesthesia was used as a means of restraint (even if no pain is

involved) such as for radiography, when manual restraint is not allowed for reasons

of personal safety.

General anaesthesia implies the loss of consciousness so that awareness is

lost and events can not be recalled. Drugs which induce general anaesthesia may be

administered intravenously, intramuscularly, or by inhalation. Choice of the

technique is influenced by facilities available, skill and experience of the

19

anesthetist, the temperament of the animal, the species, breed, age, health of the

animal, nature and duration of the surgical operation.

The disadvantages to inhalant anaesthesia are the complexity and cost of the

equipment needed to administer the anesthesia, and potential hazards to personnel.

All inhalant drugs are volatile liquids; they should not be stored in animal rooms

because the vapors are either flammable or toxic to inhale over extended periods of

time. In particular, ether must be stored in a proper hood or cabinet designed for

flammable materials. Intravenous anaesthesia (IVA) is now well established in

most areas of anaesthetic provision and is the preferred technique in the eyes of

some practitioners.

In Sudan and many other third world countries, Veterinary anaesthesia and

inhalation anesthesia in particular is still lagging behind because of unavailability

of anaesthetic drugs, the lack of continuous financial support for anaesthetic

practice and training and the lack of sophisticated equipment such as anaesthetic

machines and their accessories as well as the lack of servicing facilities to these

equipment.

Taking into consideration the above mentioned problems facing inhalation

anaesthesia in Sudan and many other third world countries, total intravenous

anaesthesia will still have a vital role to play particularly under field conditions

where no inhalation anaesthetic facilities are available.

In Sudan, Ghurashi, (1999) conducted experiments in healthy desert goat

kids using Thiopentone sodium (2.5%) at three different dose levels viz: 10, 15 and

20 mg/kg, he suggested that increasing Thiopentone sodium dose resulted in an

increase in the duration of the different anaesthetic phases. Respiration and heart

rate were affected significantly (p<0.05) as a result of using Thiopentone sodium at

20

the three different levels, while rectal temperature was affected non-significantly in

the three groups.

Nuha (2004), conducted other experiments in Nubian goat kids using

combined protocols of Thiopentone or Ketamine with premedications (Xylazine or

Medetomidine), antidote Atipamizole and local analgesic Lidocaine, her results

showed that there was non significant changes in respiratory rate following

induction of anaesthesia with 4 protocols out of 6 protocols tested. Apnoea

occurred only in association with protocol Thiopentone sodium-Xylazine.

Significant bradycardia occurred in association with all protocols tested except the

protocol Thiopentone sodium-Xylazine. Rectal temperature was significantly

dropped when Thiopentone sodium was used as an induction agent in Xylazine

premedicated animals, and when Medetomidine was used in combination with

Ketamine.

Batoul, (1990), studied general anaesthesia in goats with Thiopentone

sodium (5%) at dose rate 20 mg/kg body weight. and its effects on some

haematological parameters.

Objectives of this study:

1. To evaluate selected intravenous anaesthetic protocols for use in desert

female goats.

2. To study the effects, if any, of the selected anaesthetic protocols on some

physiological parameters of desert goats.

3. To compare and contrast the results obtained using the different selected

anaesthetic protocols.

21

CHAPTER ONE

22

CHAPTER ONE

Literature review

1. Intravenous anaesthesia in goats

Anaesthesia is an indispensable pre-requisite to most of the surgical

interventions, both in humans and animals, so that the surgeon can perform surgical

intervention with maximum precision and sagacity. Anaesthetics are available for

both parenteral as well as inhalation routes. In the developing countries total

intravenous anaesthesia still represents a good choice for surgical interference and

this may be due to complexity and cost of the equipment needed to administer the

inhalation anesthesia. As well as in Sudan, due to meager facilities available for

field veterinarians. In Pakistan intravenous anaesthetics are preferred, because of

their early and safe induction (Muhammad, Zafar, Muhammad, Masood, Manzoor,

and Sarfaraz, 2009).

Injectable anaesthetics are distinguished from inhalation anaesthetics (gases

or volatile liquids) in being solid compounds which may be dissolved in water,

solubilized by incorporating water- based preparations suitable for intravenous,

intramuscular and occasionally intraperitoneal injection or other parenteral route

(Brander, Pugh, Bywater, and Jenkins, 1991). The ideal intravenous anaesthetic

agents should be water soluble, stable (in solutions or when exposed to light over a

long time), have no damage to venous or body tissues, has short action and it's

inactivation is carried out through metabolism, have nontoxic metabolites, no

histamine release and minimal harmful cardiorespiratory effects (Dundee, 1978).

Each of Injectable anaesthetics has side effects and none of them was regarded as

ideal (Brander et al., 1991).

Sedation and general anaesthesia in sheep and goats is usually uncomplicated

except notable regurgitation with potentially fatal pulmonary aspiration (Hall,

23

Clarke and Trim, 2001). In addition, Ghurashi, (1999) reported that, salivation,

tympany and regurgitation of rumen contents are the chief difficulties during

general anaesthesia in ruminants.

1.1. Thiopentone sodium (thiopental)

Thiopentone sodium was introduced into Veterinary practice in UK in 1973

(Hall et al., 2001). It's known as an ultra short-acting barbiturate (Susan and

Donald, 2003; Hall et al., 2001).

1.1.1 Identity

Thiopentone sodium is a mixture of mono sodium salts usually available as

powder to be dissolved in water before use (Hall et al., 2001). It is a white to

yellowish, crystalline powder, odorless, soluble in water, alcohol and highly

soluble in lipids. Commercially available drug for injection contains anhydrous

sodium carbonate as a buffer. The powder stored at a controlled room temperature

of 15–30°C (AHFS, 2005). Because of its irritant effect, Thiopentone sodium must

be injected intravenously (Hall et al., 2001).

1.1.2. Chemical name

It is a 5- ethyl -5- (1-methyl butyl) -2- thiobarbiturate (100 parts w/w) and

exsiccated sodium carbonate (6 parts w/w) (Vickers, Shnienden, and Wood-Smith,

1984)

1.1.3. Molecular formula

Its molecular formula is C12H19N2 Na O2S

1.1.4. Mode of action

Thiopentone sodium binds at a distinct binding site associated with a Cl-

ionopore at the gamma amino butric acid (GABA) receptor increasing the duration

of time for which the Cl- ionopore is open (Olsen, 1981). The post-synaptic

inhibitory effect of GABA in the thalamus is, therefore, prolonged.

24

Figure 1.1 Chemical structure of Thiopentone sodium

25

1.1.5 Pharmacology

Induction doses of this drug are usually between 5 and 10 mg/kg for use in

most species (Hall et al., 2001), and 1.25%, 2.5%, 5% solutions are used in most

animals depending on animal's size (Thurmon, Tranquilli, Benson, and Lumb,

1996).

The duration and depth of anaesthesia due to injection of Thiopentone

sodium depend on the amount of the injected drug, speed of injection, rate of

distribution of the drug in the non-fatty tissues of the body, rate of uptake of the

drug by the body fat, and using of premedication (Batoul, 1990; Rawling and

Kolata, 1983; Hall et al., 2001). Thiopentone sodium appears to cross the blood-

brain barrier with very great speed and after intravenous injection it rapidly reaches

the central nervous system and its effects become apparent within 15 - 30 seconds

(Hall et al., 2001). Susan and Donald, (2003) reported that Thiopentone sodium is

highly soluble in lipid, and rapidly enters the CNS producing profound hypnosis

and anesthesia, and then redistributes to muscle and adipose tissue in the body. The

short duration of action of this agent is due to redistribution out of the CNS and

into muscle and fat stores less than to rapid metabolism, so Greyhounds and other

sight hounds may exhibit longer recovery times than other breeds. This may be due

to their low body fat levels or differences in the metabolic handling of the

thiobarbiturates (Susan and Donald, 2003). After a single dose, concentration of

Thiopentone sodium rises highly in plasma and liver immediately after injection

and soon fell rapidly. Also muscle concentration rises high immediately after

injection, but continued to rise for some 20 minutes, then fells rapidly during the

first hour then becomes progressively slower in the next two to three hours.

Concentration of this agent in the body fat neglected immediately after injection,

then increased rapidly during the first hour, and then more slowly until reached its

26

maximum in three to six hour after single dose injection (Hall et al., 2001). Rapid

intravenous injection of an initial dose of Thiopentone sodium in a dose rate of 15 –

20 mg/kg in a concentration of 5%, produces anaesthesia and 30 – 50 seconds of

apnoea in goats (Hall and Clarke, 1983). Several metabolites have been isolated

after metabolism of Thiopentone sodium through the hepatic microsomal system

and very little of the drug is excreted unchanged in the urine (Susan and Donald,

2003; Thurmon et al., 1996). Recovery from Thiopentone sodium anaesthesia is

reported to be quick and quiet (Hall and Clarke, 1991).

1.1.6. Toxic effects

Depression of the respiratory center was reported to be as the main toxic

effect of Thiopentone sodium (Hall et al., 2001). Significant vascular dilatation

and hypoglycemia were observed when Thiopentone sodium is injected too rapid

intravenously (Susan and Donald, 2003). Cats are susceptible to developing apnoea

after injection and may also develop a mild arterial hypotension (Susan and

Donald, 2003). In goats, injection of Thiopentone sodium causes tachycardia at

different times (Contreras and Aspe, 1992).

Batoul, (1990), studied general anaesthesia in goats with Thiopentone

sodium (5%) at dose rate of 20 mg/kg body weight and its effects on some

haematological parameters. She reported that general anaesthesia when applied

once caused a decrease in the number of red blood cells (RBCs) and increase in

mean cell volume (MCV), when compared with pre-trial values. Repeated general

anaesthesia for three successive days, affect the values of Haemoglobin (Hb),

Packed Cell Volume (PCV) and (MCV) with significant decrease in values. Total

number of White Blood Cells (WBCs) was not affected. The number of

Neutrophils was significantly decreased and monocytes were increased.

27

1.1.7. Use of Thiopentone sodium in goats

Anaesthetic induction dose of Thiopentone sodium is 7- 20 mg/kg in the

unpremedicated animal, but recommended initial dose is 5 – 7 mg/kg of 2.5%

solution to avoid overdose in goats (Hall et al., 2001).

Ghurashi, Sobair, Seri, and Ashwag, (2007) studied some physiological and

anaesthetic effects of this drug at dose rate of 10 mg/kg administered intravenously

in goat kids premedicated with acepromazine or diazepam or Xylazine and non

premedicated animals. They suggest that the use of premedication prior to

thiopentone sodium lead to smooth induction of anaesthesia rather than non

premedicated animals. They also reported that physiological parameters

(respiratory rate, heart rate and rectal temperature) were affected to different limits,

and the usage of premedications especially xylazine lead to improvement of

Thiopentone sodium anaesthetic effects.

1.2 Ketamine Hcl (Ketalar)

Ketamine hydrochloride is a dissociative anaesthetic and a member of the

phencyclidine group. It is a short acting anesthetic agent being widely used in

recent years. It is developed in 1963 to replace phencyclidine and is being currently

used for human and veterinary anesthesia (Tanaka, Honda, Yasuhara, 2005).

Ketamine is a cardiovascular stimulant and it has been used for spinal analgesia in

humans (Bion, 1984) and animals (Aithal, Amarpal, and Singh, 1996; Gomez de

Segura, 1998; DeRossi, Junqueira, Lopes, and Beretta, 2005). Ketamine is used for

premedication, sedation, induction and maintenance of general anaesthesia (Sinner

and Graf, 2004; Huai-Chia, Ta-Liang, and Ruei-Ming, 2009; Rose, Matthias,

Saskia, Michael, Andreas, Gunter, Horst, and Andrea, 2005).

28

1.2.1 Identity

The drug is a water and lipid soluble, allowing it to be administered

conveniently via various routes and providing extensive distribution in the body

(Sinner and Graf, 2004). The drug is manufactured as injectable odorless and

tasteless liquid (Tanaka, et. al., 2005).

1.2.2 Chemical name

It is a 2-(o-chlorophenyl)-2- methylamino)- cyclohexanone.

1.2.3 Molecular formula

Its molecular formula is C13 H18 N O Cl

1.2.4 Mode of action

Ketamine was originally presented as a racemic mixture of two isomers (S+

and R–). The (S+) isomer is 3–4 times as potent as an analgesic with a faster

clearance than (R–) (Sneyd, 2004; Sinner and Graf, 2004; Rose et al., 2005). This

drug acts on a variety of receptors, including nicotinic (Scheller et al., 1996),

muscarinic (Hustveit et al., 1995; Sinner and Graf, 2004), and opioid receptors

(Finck and Ngai, 1982; Smith et al., 1987; Hustveit et al., 1995; Sinner and Graf,

2004) and affects the N-methyl-d-aspartate (NMDA) receptor complex channel as a

noncompetitive antagonist at the phencyclidine receptor site (Yamamura et al.,

1990; Sinner and Graf, 2004). Rose and his team (2005) concluded that Ketamine

blocks Na+ and K+ channels in superficial dorsal horn neurons of the lumbar spinal

cord there by reducing the excitability of the neurons, which may play an important

role in the complex mechanism of its action during spinal anaesthesia.

1.2.5 Pharmacology

Ketamine can be administrated via intramuscular or intravenous route (Hall

et al., 2001), epidurally in goats (Aithal et al., 1996). Thurmon et al., (1996)

reported that unconsciousness and analgesia due to injection of Ketamine are dose

29

Figure 1.2 Chemical structure of Ketamine

30

related. This drug produces analgesia (without muscle relaxation) and increase

salivation (Hall et al., 2001). Sinner and Graf, (2004) stated that Ketamine causes

bronchodilation, stimulation of the sympathetic nervous system and cardiovascular

system. Ketamine crosses the brain blood barrier rapidly and because of its brain /

plasma ratio becomes constant in less than one minute, the onset of action is rapid

(Hall et al., 2001). Ketamine metabolism is mediated by hepatic microsomal

enzymes, and excreted as four metabolites in the urine (Hall et al., 2001; Sinner

and Graf, 2004).

1.2.6 Toxic effects

Impaired motor function, high blood pressure, depression and potentially

fatal respiratory suppression were reported to be the most toxic effects of Ketamine

Hcl (Tanaka et al., 2005).

1.2.7 Use of Ketamine Hcl in goats

Without fear of causing convulsion, Ketamine Hcl can be used in sheep and

goats, and muscle relaxation due to its administration is poor (Hall et al., 2001).

Ketamine has been acclaimed on account of its safety and its favourable effects

upon cardiovascular and respiratory systems and because of its sympathomimetic

and antiarrhythmic properties, it is useful in poor-risk and hypovolaemic patients

(Idvall, Ahlgren, Stenberg, 1979). Ketamine produce stage of sedation with

profound analgesia and partial depression of cough and swallowing reflexes (Hall

et al., 2001).

1.3 Diazepam

Diazepam is probably the most widely used of the benzodiazepines (Hall et

al., 2001). It is one of the most widely prescribed drugs in the world. Clinically

Diazepam is administers prior to general anaesthetics as psychoseditive

premedication for endoscopic and bronchoscopic procedures, as anticonvulsant to

31

control intractable seizure activity and as an anxiolytic to moderate anxiety and

agitation (Sellers, 1978). Premedication with diazepam increase the length of action

of other anaesthetic agents and the drug is particularly useful prior to Ketamine

anaesthesia to reduce the hallucinations which seem to be associated with Ketamine

anaesthesia (Hall et al., 2001). Marrs (2004) reported that, diazepam is indicated in

convulsions or pronounced muscle fasciculation caused by organophosphorus

insecticides poisoning.

1.3.1 Identity

Diazepam is a white to yellow, tasteless initially, but a bitter after-taste

develops, odourless crystalline powder with a melting point between 131-135°C

(Susan and Donald. 2003; Marrs, 2004). The drug is insoluble in water and

solutions for injections contain solvents such as propylene glycol, ethanol and

sodium benzoic acid (Hall et al., 2001). One gram is soluble in 333 ml of water, 25

ml of alcohol, and it is sparingly soluble in propylene glycol. The pH of the

commercially prepared injectable solution is adjusted with benzoic acid/sodium

benzoate to 6.2-6.9. It consists of a 5 mg/ml solution with 40% propylene glycol,

10% ethanol, 5% sodium benzoate/benzoic acid buffer, and 1.5% benzyl alcohol as

a preservative (Susan and Donald. 2003; Marrs, 2004). Diazepam should not be

mixed with other drugs in the same infusion solution or in the same syringe as there

are numerous incompatibilities (Trissel, 2003).

1.3.2 Chemical name

It is a 7-chloro-1, 3-dihydro-1-methyl-5-phenyl-2H-1, 4-benzodiazepin-2-

one (Marrs, 2004).


Diazepam molecular formula is C16H13ClN2O

32

Figure 1.3 Chemical structure of diazepam

33


The action of benzodiazepine compounds is thought to be through

stimulation of specific benzodiazepine (BZ) receptors (Hall et al., 2001). Their

main sedative effects are through depression of the limbic system, and their muscle

relaxing properties are through inhibition of the internuncial neurones at spinal

levels (Hall et al., 2001). Susan and Donald (2003) reported that the exact

mechanism of action is unknown, but postulated mechanisms include: antagonism

of serotonin, increased release of and/or facilitation of gamma-aminobutyric acid

(GABA) activity, and diminished release or turnover of acetylcholine in the CNS.

1.3.5 Pharmacology

Diazepam can be administered intravenously, intramuscularly, orally and

rectally via suppository or enema (Barbara Forney, 2002). The sub cortical levels

(primarily limbic, thalamic, and hypothalamic) of the CNS are depressed by

diazepam producing the anxiolytic, sedative, skeletal muscle relaxation, and

anticonvulsant effects (Susan and Donald, 2003). After oral administration

Diazepam is rapidly absorbed and reached peak plasma levels within 30 minutes to

2 hours. However it was slower than oral and incompletely absorbed following

intramuscular administration (Susan and Donald, 2003). Diazepam is metabolized

by the liver to nordiazepam and other active metabolites which are excreted in the

urine (Barbara Forney, 2002).

1.3.6 Toxic effects

Intravenous injection of diazepam may cause thrombophlebitis and this is

thought to be due to the solvent rather than to diazepam itself (Hall et al., 2001).

1.3.7 Use of Diazepam in goats

Diazepam when injected intravenously and alone in sheep and goats may

produce some sedation and ataxia for 15 – 30 minutes, but the degree of sedation is

34

unpredictable in healthy animal (Hall et al., 2001). At dose rate of 0.2 mg/kg

intravenously injected Diazepam can be used to produce mild sedation for

transdermal tracheal wash (Hall et al., 2001).

1.4 Xylazine

Xylazine is the most widely used agent for chemical restraint in ruminants

including goats. It has sedative, analgesic and muscle relaxing properties. It has a

wide acceptance because of good tolerance and the optional intramuscular and

intravenous administration (Ndeereh, Mbithi, and Kihurani, 2001). Xylazine is a

powerful tranquilliser, which is commonly used to sedate large animals especially

prior to surgical procedures. Anaesthetic effects and muscle relaxing properties

may vary in intensity depending on the administrating dose (Spyridaki, Lyris,

Georgoulakis, Kouretas, Konstantinidou, and Georgakopoulos, 2004). It is

commonly used alone or in combination with other sedatives, analgesic or

anaesthetic agents. Though Xylazine is relatively safe to use in ruminants,

prolonged recovery is not uncommon, especially when high dose rates were used

(Knight, 1980).

1.4.1 Identity

Xylazine is an organic base which is administered as an aqueous solution of

hydrochloride salt (Brander et al., 1991).

1.4.2 Chemical name

It is a 2(2, 6-dimethyl phenylamino) - 4H - 5, 6 – dihydro - 1, 3 – thiazine -

hydrochloride) (Thurmon et al., 1996).


Xylazine molecular formula is C12H16N2S

35

Figure 1.4 Chemical structure of Xylazine

36


Xylazine stimulates directly peripheral α2-adrenergic receptors located in

various tissues (Kobinger, 1978). Prolonged analgesia, with a long duration of

action observed when Xylazine injected into the subarachnoid space, is mediated

by the α2-adrenergic receptors located in the dorsal horn of the spinal cord. Muscle

relaxation due to Xylazine was reported to be through inhibition of intraneural

transmission of impulses in the central nervous system (Thurmon et al., 1996).

1.4.5 Pharmacology

This drug can be used in all domestic animals with various doses (Brander et

al., 1991). It can be administrated by intravenous, intramuscular, or subcutaneous

routes (Hall et al., 2001), and spinally in goats (Kinjavdekar, Singh, Amarpal,

Aithal, and Pawde, 2007). Intramuscular injection of Xylazine at 0.44 mg/kg

produced continued recumbency, analgesia and marked sedation at approximately

10 minutes (Ndeereh et al., 2001). Reduction of the recovery period in sedated

ruminants would minimize risks of such complications, ruminants (especially

goats) require small doses of Xylazine with an agent to reverse the effects of

Xylazine would be useful for treating accidental overdose (Ndeereh et al., 2001).

Analgesic and sedative effects of Xylazine can be reversed with α2 adrenoceptors

antagonists (Brander et al., 1991). There are marked variations in susceptibility to

Xylazine between the various species of domestic animals. Horses, dogs and cats

require 10 times the dose needed in cattle. Pigs are even more resistant than horses

(Hall et al., 2001). It is possible that lesser variations in sensitivity may occur in

breeds within a single species and this might contribute to the occasional failure of

the drug to produce sedation (Hall et al., 2001). Xylazine is metabolized in the liver

and excreted via kidneys (Hall and Clarke, 1983).

37

Xylazine causes sedation primarily by stimulating the central nervous system

presynaptic α2-adrenergic receptors. It produces a profound hypertensive response

within 15 seconds after injection. It also depresses cardiac minute work,

mechanical index of myocardial oxygen demand and coronary blood flow in a

similar manner (Spyridaki et. al., 2004).

Xylazine is absorbed, metabolised and eliminated extremely rapidly. It is

metabolised to many different compounds, the final breakdown products being

organic sulphates and carbon dioxide. The pharmacokinetic disposition of xylazine

hydrochloride has been described after both intravenous and intramuscular

injection in horse, cattle, sheep and dog. In the horse, following an intravenous

administration, the maximum sedative effect occurs within 4–8 minutes after

injection. Following an intramuscular administration, sedation is usually evident

within 10 minutes and reaches its maximum effect by 15 minute. Thus, in horses,

clinical and pharmacokinetic data suggest that Xylazine itself, and not a metabolite,

is the active drug (Garcia-Villar, Toutain, Alvinerie, and Ruckebusch, 1981;

Spyridaki et. al., 2004). The main pathway of biotransformation is most likely via

1-amino-2,6- dimethylbenzene, which is formed when the thiazine ring breaks

down (Spyridaki et. al., 2004).

1.4.6 Toxic effects

Xylazine causes marked hypertension and bradycardia in dogs and cats,

sweating in horses and in late pregnancy lead to premature delivery in cattle

(Brander et al., 1991). At the time of maximum sedation, the aspiration pneumonia

and pressure damage to nerves and muscles may arise due to prolonged recovery

periods of Xylazine. Also pronounced salivation and/or excessive depression of the

central nervous, cardiovascular, respiratory and gastrointestinal systems were

reported as Xylazine complications (Taylor, 1990).

38

1.4.7 Use of Xylazine in goats

Dose rate for Xylazine in goats range from 0.02 to 0.2 mg/kg in which

Xylazine provides light to heavy sedation according to the dose rate administered.

Use of this agent alone provide satisfactory sedation for restraint or can be used for

premedication prior to induction of anaesthesia with other agents (Hall et al.,

2001).

Intravenous injection of xylazine Hcl at dose rate of 0.05 mg/kg in Nubian

goat kids caused the animals to assume recumbancy position (Nuha, 2004).

1.5 Medetomidine (Domitor)

Medetomidine is a α2-adrenergic receptor agonist. It has analgesic, sedative,

and muscle relaxation properties (Mpanduji, 2001). It is highly selective, specific

and potent α2-adrenoreceptor agonist and induces more potent pharmacological

effects as compared to Xylazine (Pawde, Amarpal, Singh, and Naveen, 1996).

Premedication with medetomidine decreased anaesthetic requirements during

anaesthesia with thiopentone sodium, halothane and nitrous oxide (Bergstrom,

1988; Young and Jones, 1990), propofol and halothane (Bufalari, Short, Giannoni,

Pedrick, Hardie, and Flanders,1997), isoflurane (Kuusela, Raekallio, Väisänen,

Mykkanen, Ropponen, and Vainio, 2001; Ewing, Mohammed, Scarlet, and Short ,

1993) propofol (Vainio, 1991; Cullen and Reynoldson, 1993; Hammond and

England, 1994; Bufalari, Short, Giannoni, and Vainio, 1996), halothane (Vickers,

Sheridan, Segal, and Maze, 1988; Segal et al., 1989) in dogs. A recent study

suggests that, as a premedicant to general anaesthesia, medetomidine may possess

comparatively better potential to attenuate perioperative stress responses in dogs

than sedatives such as acepromazine (Vaisanen et al., 2002). Medetomidine has

also been used as a premedicant before general anaesthesia in rabbits, sheep and

horses (Flecknell and Liles, 1996; Kastner, Boller, Kutter, Akens, and Bettschart,

39

2001; Yamashita, Muir, Tsubakishita, Abrahamsen, Lerch, Hubbell, Bednarski,

Skarda, Izumisawa, and Kotani, 2002). In horses premedicated with medetomidine,

transition to inhalational anesthesia was smoother than those premedicated with

Xylazine (Yamashita et al., 2002).

The drug has been widely used in combination with other drugs to prolong

recumbency and the most popular combination is with Ketamine Hcl (Hall et al.,

2001). Medetomidine /Ketamine combination have been found to provide excellent

immobilization and relaxation in wide range of species of animals, while the ability

to reverse the sedation with α2-adrenoceptor antagonists has proved to be

particularly useful (Jalanka, 1989).

1.5.1 Identity

It is a white or almost white crystalline substance, soluble in water (Susan

and Donald, 2003). This drug is a racemic mixture of equal proportions of two

optical enantiomers – the levo- and dextro-rotatory optical isomers (MacDonald et

al., 1991)

1.5.2 Chemical name

Medetomidine is a 4-[1-(2, 3-dimethyl phenyl) - ethyl] 1H-imidazole (Hall et

al., 2001; Mpanduji, 2001; Pawde et al., 1996).


Medetomidine molecular formula is C13H16N2.HCl


The mode of action of Medetomidine is mainly through activation of α2

adrenoceptors (very potent, selective and specific) full agonist at pres-synaptic and

post-synaptic α2 adrenoceptors (Hall and Clarke, 1991).

40

Figure 1.5 Chemical structure of Medetomidine

41

1.5.5 Pharmacology

Medetomidine produces sedation, muscle relaxation and analgesia in dogs

(Vainio et al., 1989; Serteyn et al., 1993), cats ( Pawde et al., 1996), human beings

(Scheinin M. 1987), wild animals (Jalanka, 1990), laboratory animals (Nevalainen

et al., 1989) and Shami goat kids (Mohammed et al., 1991). The solution of

Medetomidine is not irritant and can be administrated by subcutaneous,

intramuscular, intravenously or sublingually (Hall et al., 2001).

Susan and Donald, (2003), reported that Medetomidine has rapid onset of

effect (5 minutes for IV; 10-15 minutes for IM). Also they showed that the drug

can be absorbed via the oral mucosa when administered sublingually in dogs, but

efficacy at a given dose may be less than intramuscular dosing.

Pharmacological activity of medetomidine is stereospecific and is due

predominantly to its dextro-rotatory isomer (Segal et al., 1988; Virtanen et al.,

1988).

Following subcutaneous (rat) and intramuscular (dog) administration,

medetomidine is rapidly absorbed into the blood stream and rapidly distributed into

well-perfused tissues, including the brain, effectively penetrating these tissues and

readily reaching its target receptors (Salonen, 1989). Sedation and analgesia

induced by medetomidine in animals are dose-dependent and reach ceiling points

beyond which increasing the dose may only prolong the duration of these responses

but not their intensities (Vainio et al., 1989).

Elimination occurs mainly by biotransformation in the liver, the rate of

which may be controlled by hepatic blood flow (Salonen, 1989). Medetomidine is

rapidly excreted mostly via the urine as metabolites with no pharmacological

activity, and only traces of the drug are excreted unchanged (Salonen, 1989).

42

Following an intramuscular administration of 80 µg/kg medetomidine in

cats, absorption occurred rapidly. Peak serum concentration (24.6 ng/ml) was

reached within 15 minutes of drug administration and absorption half-life was 8

minutes (Salonen, 1989). Distribution occurred rapidly and tissue penetration was

effective (Salonen, 1989). The apparent volume of distribution was found to be 3.5

l/kg and most of the drug existed in circulation in its inactive protein-bound form,

with only 15% remaining as a free fraction (Salonen, 1989). Half-life of

elimination was 1.35 hrs and total clearance was 29.5 ml/min kg (Salonen, 1989).

About two-thirds of the original dose of drug was excreted via urine, mostly as

pharmacologically inactive metabolites during the first 24 hrs after dosing, with

very little found in faeces (Salonen, 1989). Unlike in other animals, cat urine

contained no or negligible amounts of β-glucuronidase hydrolysable conjugates

(Salonen, 1989).

1.5.6 Toxic effects

The drug decreases body temperature, heart rate, and respiratory rate and

increase mean arterial blood pressure, cortisol and glucose in goats (Gwendolyn el

al., 2005). Sakamoto and others (1997) suggested that, in late pregnant goats,

Medetomidine induced a decrease in maternal cardiac output, a decrease in

intrauterine pressure (IUP) arising from the induction of uterine contractions, and

transplacental Medetomidine can have a suppressive effect on the fetus (transient

decrease and increase in the fetus heart rate and arterial blood pressure

respectively).

1.5.7 Use of Medetomidine in goats

Medetomidine provides light to heavy sedation according to the dose rate

administered. The use of this agent alone provides satisfactory sedation for restraint

or can be used for premedication prior to induction of anaesthesia with other agents

43

(Hall et al., 2001). After Medetomidine was administered in goats, recumbency

occurred 89 ± 50 seconds after administration (Gwendolyn el al., 2005).

In Nubian goats, intravenous injection of medetomidine Hcl at dose rate of

10 µg/kg caused the animals to assume recumbancy position (Nuha, 2004).

44

CHAPTER TWO

45

CHAPTER TWO

Materials and methods

2.1. Place of study

This study was conducted at the premises of the Department of Clinical

Studies, Faculty of Veterinary Science, University of Nyala, South Darfur, Sudan.

2.2 Experimental animals

A total number of sixty four adult female desert goats, their ages ranging

between 2 – 3 years, and weighing between 17 – 25 kilograms were used in this

study. Animals were randomly allocated to eight groups of equal size. Before the

start of the experiments the animals were examined clinically to prove freedom

from diseases. The animals were kept half grazing at the University of Nyala farm

with complementary feeding was provided in pens at night.

2.3 Drugs

Three pre-anaesthetic medications and two anaesthetics were used and they

were as follows:

1. Diazepam (0.5%) (Shanghai pharmaceutical company (SHAPHAR), China) as

shown in figure (2.1).

2. Xylazine Hcl (Rompun 2%, alfasan, Holland) Figure (2.1).

3. Medetomidine Hcl (Domitor 0.1%, Rion pharma, Finland) Figure (2.1).

4. Ketamine Hcl (5%, USA, TRITTAU, Germany) Figure (2.2).

5. Thiopentone sodium (THIOSOL, B.P, 500mg, India) Figure (2.2).

2.4 Injection set

Disposable syringes 1, 5, and 10 ml, 21 to 24 G (ELASHER, EGYPT), and

intravenous catheters (21G) were used for intravenous injection of drugs (Figure

(2.3).

46

A = Xylazine, B = Medetomidine (Domitor), C = Diazepam

Figure (2.1) Pre-anaesthetic medications used in different protocols

A B C

47

A = Thiopental, B = Ketamine Hcl

Figure (2.2) The intravenous anaesthetic drugs used in the different protocols

A B

48

A = size 1 ml plastic syringe, B = size 1 ml glass syringe, C = size 5 ml plastic

syringe, D = intravenous catheter

Figure (2.3) Syringes with different size levels used in performing anaesthetic

protocols

A B C D

49

A = Phonendoscope (stethoscope), B = Digital thermometer

Figure (2.4) Monitoring tools used for monitoring physiological parameters

tested

A B

50

2.5 Monitoring tools

Phonendoscope (stethoscope) was used for monitoring heart rate,

Observation of abdominal movements and/or Phonendoscope (stethoscope) were

used for monitoring respiration. Digital thermometer was used for monitoring rectal

temperature. Stop watch was used to determine the length of different phases of

anaesthesia and monitoring reflexes every 10 minutes (Figure, 2.4)

2.6 Anaesthetic protocols

Eight different anaesthetic protocols were tested in this investigation as

follows:

1. Ketamine Hcl (KT) at dose rate 4 mg/kg (without premedication).

2. Thiopentone sodium (TH) 2.5% at dose rate 10mg/kg (Without premedication).

3. Diazepam 0.5 mg/kg + Ketamine at dose rate 4 mg/kg (KT-DI).

4. Xylazine 0.1 mg/kg + Ketamine Hcl 4 mg/kg (KT-XY).

5. Medetomidine 10 µg/kg + Ketamine Hcl 4 mg/kg (KT-ME).

6. Diazepam 0.5 mg/kg + Thiopentone sodium (2.5%) at dose rate 10 mg/kg (TH-

DI).

7. Xylazine (2%) 0.1 mg/kg + Thiopentone sodium (2.5%) at dose rate 10 mg/kg

(TH-XY).

8. Medetomidine 10 µg/kg + Thiopentone sodium (2.5%) at dose rate 10 mg/kg

(TH-ME).

2.7 Experimental design

Each of the above mentioned protocols was tested in eight animals. The

jugular vein was used for injecting all drugs using intravenous catheter. To start

each of the premedication containing protocols (group 3 to group 8), animals were

injected with one of the selected premedications (Diazepam, Xylazine or

Medetomidine) slowly intravenously, followed after 10 minutes with a rapid

51

intravenous injection of one of the selected anaesthetics (Ketamine Hcl or

Thiopentone sodium), as follows:

2.7.1 First experiment

Animals in this group received rapid intravenous injection of Ketamine Hcl

(4 mg/kg) without premedication.

2.7.2 Second experiment

This group of animals received rapid intravenous injection with Thiopentone

sodium (2.5%, at dose rate of 10 mg/kg) without premedication.

2.7.3 Third experiment

Animals in this group received slow intravenous injection of Diazepam (as a

premedication) (0.5 mg/kg), followed after ten minutes by rapid intravenous

injection of Ketamine Hcl (4 mg/kg).

2.7.4 Fourth experiment

In this group, animals were injected slowly via intravenous route with

Xylazine (0.1 mg/kg) as a premedication, anaesthesia was then induced after ten

minutes by rapid intravenous injection of Ketamine Hcl (4 mg/kg).

2.7.5 Fifth experiment

Another group of eight animals was injected slowly through intravenous

route with Medetomidine (10 µg/kg) as a premedication, followed after ten minutes

by rapid intravenous injection of Ketamine Hcl (4 mg/kg).

2.7.6 Sixth experiment

A group of eight animals received a slow intravenous injection with

Diazepam (0.5 mg/kg) as premedication, followed after ten minutes by rapid

intravenous injection of Thiopentone sodium (10mg/kg).

52

2.7.7 Seventh experiment

A group of eight animals was injected slowly via intravenous route with

Xylazine (0.1 mg/kg) as a premedication, followed after ten minutes by rapid

intravenous injection of Thiopentone sodium (10 mg/kg).

2.7.8 Eighth experiment

A group of eight animals was injected at slow rate through intravenous route

with Medetomidine (10 µg/kg) as a premedication, followed after ten minutes by

rapid intravenous injection of Thiopentone sodium (10 mg/kg).

Each group of animals was monitored before anaesthesia, during anaesthesia

and till recovery occurred.

2.8 Physiological parameters

Physiological parameters were monitored at 10 minutes intervals using

standard methods as described by Kelly (1984) as follows:

2.8.1 Respiratory rate

Observations of abdominal movements and/or Phonendoscope (stethoscope)

were used for monitoring respiration.

2.8.2 Heart rate

Phonendoscope (stethoscope) was used for monitoring the heart rate through

the left 3 rd – 5th intercostal spaces.

2.8.3 Rectal temperature

Digital thermometer as used for monitoring rectal temperature. The

thermometer bulb was lubricated with lubricant jell then inserted into the empty

rectum as described by Kelly (1984).

53

2.9 Phases of anaesthesia

2.9.1 Induction phase

It is the state or condition in which the animal start becomes unconscious,

not responding to painful stimuli with disappearance of selected reflexes (Jani et

al., 1982)

2.9.2 Anaesthetic phase

Was considered as the period during which the animal showed signs of

unconsciousness, no reflexes and not responding to painful stimuli (Tamisto et al.,

1981).

2.9.3 Basal narcosis

Was assessed as the period during which the animal shows signs of

unconsciousness, but response positively to noxious or painful stimuli (Atkinson,

Rashman, and Alfredlee, 1987).

2.9.4 Lateral recumbancy

Was considered as the duration at which the animal opens its eyes and

reflexes were regained but it is incapable of adopting sternal position (Thurmon et

al., 1996).

2.9.5 Sternal recumbancy

Was considered as the period during which the animal could adopt sternal

recumbancy without falling to lateral recumbancy and without adopting standing

position (Ghurashi, 1999)

2.9.6 Standing phase

It is the stage at which the animal can stand but unable to walk ten steps

(Ghurashi, 1999)

54

2.9.7 Recovery

The animal was considered to be recovered from anesthesia when it is cable

of supporting itself in standing position and walk for ten steps without falling down

(Ghurashi, 1999).

2.9.8 Total recovery

Total recovery time was considered as the total time calculated from the time

of induction of anesthesia until recovery was attained (Nuha, 2004).

2.10 Reflexes

2.10.1Tongue reflex

Was assessed by pulling the tongue outside the mouth, when the animal was

capable to pull its tongue into the mouth, the reflex was considered positive (Nuha,

2004).

2.10.2 Palpepral reflex

The reflex was assessed by digital touch on the canthus or eyelashes, if

purposeful motor reflex observed, the reflex was consider positive as reported by

Batoul, (1990).

2.10.3 Swallowing reflex

External digital pressure on the larynx was used to assess Swallowing reflex.

Positive response was considered when swallowing or laryngeal movements were

observed (Rawling and Kolata, 1983).

2.10.4 Pedal reflex

Pedal reflex was assessed by gentle pressure on the animal fore digit. If the

animal moves its leg or leg muscle, the reflex was considered positive.

55

2.10.5 Jaw relaxation reflex

Persistence of open mouth due to induced jaw retraction was considered to

be a positive jaw relaxation reflex. The reflex was considered regained when the

animal was reluctant to open its mouth.

2.10.6 Anal reflex

Anal reflex was assessed by inducing tension of anal sphincter with two

fingers. Positive response was considered when the movement of the anal sphincter

was observed.

2.10.7 Cough reflex

Gentle digital pressure on the first 3rd tracheal cartilage was used to assess

Cough reflex. Positive response was considered when the cough was induced

(Blood and Henderson, 1994).

2.11 Statistical analysis

For physiological parameters (Respiratory rate, Heart rate and Rectal

temperature) comparison, T- test was used to compare means, while ANOVA was

used for compare and contrast between the different anaesthetic phases using SAS

System computer package.

56

CHAPTER THREE

57

CHAPTER THREE

Results

3.1. Effects of different anaesthetic protocols on the respiratory rate, heart

rate and rectal temperature:

When Ketamine Hcl was used without premedication as shown in table (1)

we observed that, there was significant (P≤0.05) increase in the respiratory rate at

times (0, 10, and 20) minutes and a significant decrease (P≤0.05) in 40 minute

following induction of anaesthesia, while there is no significant change in heart rate

or rectal temperature observed during Ketamine Hcl anaesthesia.

When Ketamine was used with diazepam as shown in Table (2) there was

non significant (P≥0.05) decrease in the respiratory rate at times (0, 10, 30 and 40)

minutes and a non significant (P≥0.05) increase at time 20 minute following

induction of anaesthesia. The heart rate increased non significantly at times (10 and

20) minutes. Also the rectal temperature expressed non significant change.

The use of Ketamine with Xylazine as shown in table (3) induced significant

increase (P≤ 0.05) in the respiratory rate which was observed at time 10 minutes

and a significant (P≤0.05) decrease was also observed at time 30 minutes following

induction of anaesthesia, while the heart rate and rectal temperature remained

without any significant change.

As shown in table (4), the combination of Ketamine with Medetomidine,

induced a significant (P≤0.05) increase in the respiratory rate at time (10 and 40)

minutes following induction of anaesthesia, while the heart rate and rectal

temperature showed non significant changes.

58

Table (1) Effects of Ketamine Hcl on physiological parameters (respiratory rate, heart rate and rectal temperature)

during the course of anaesthesia Parameters Time (minutes)

Base line value 0 10 20 30 40 50

Respiratory rate 25.3±1.5 38±4.0* 31.8±3.6* 33.5±4.3* 33.1±3.6 20.4±3.7* 30.7±3.4

(breath/min)

Heart rate 82.8±6.6 84.4±8.5 91.5±6.8 86.5±5.3 83.4±5.4 80.4±3.9 78.4±3.4

(beat/min)

Rectal temperature 39.3±0.16 39.3±0.14 39.5±0.15 39.5±0.18 39.7±0.19 39.6±0.19 39.6±0.2

(°C)

Values are mean ± Standard error of mean of eight replicates each * P ≤ 0.05

59

Table (2) Effects of protocol KT-DI on physiological parameters (respiratory rate, heart rate and rectal temperature)

during the course of anaesthesia Parameters Time (minutes)

Base line value 0 10 20 30 40

Respiratory rate 22.6±1.4 16.8±2.3 15.50±2.2 27.0±4.8 22.2±2.55 22.0±6.0

(breath/min)

Heart rate 60.5±3.3 78.3±7.3 78.3±9.4 76.3±9.4 66.7±6.0 67.0±1.0

(beat/min)

Rectal temperature 38.0±0.32 38.7±0.34 38.6±0.33 38.6±0.23 38.4±0.17 37.4±11.22

(°C)

Values are mean ± Standard error of mean of eight replicates each

60

Table (3) Effects of protocol KT-XY on physiological parameters (respiratory rate, heart rate and rectal

temperature) during the course of anaesthesia Parameters Time (minutes)


Respiratory rate 28.5±2.7 24.4±5.6 39.6±7.1* 27.8±5.1 26.5±6.1* 27.4±5.3 30.0±6.7

(breath/min)

Heart rate 73.3±4.8 69.4±5.2 60.3±3.9 56.5±3.1 60.8±2.8 60.4±3.4 59.5±3.7

(beat/min)


(°C)

Values are mean ± Standard error of mean of eight replicates each *P ≤ 0.05

61

Table (4) Effects of protocol KT-ME on physiological parameters (respiratory rate, heart rate and rectal

temperature) during the course of anaesthesia Parameters Time (min)


Respiratory rate 22.0±1.1 20.0±2.3 29.3±5.5*** 18.3±2.1 17.5±2.0 25.3±5.9*** 22.3±1.3

(breath/min)

Heart rate 90.5±5.1 77.3±3.5 76.0±3.9 70.8±3.5 66.0±3.2 67.3±3.4 70.5±2.6

(beat/min)


(°C)

Values are mean ± Standard error of mean of eight replicates each ***P ≤ 0.0001

62

Figure (3.1) Effects of Ketamine Hcl on physiological parameters (respiratory rate, heart rate and rectal

temperature) during the course of anaesthesia

63

Figure (3.2) Effects of protocol KT-DI on physiological parameters (respiratory rate, heart rate and

rectal temperature) during the course of anaesthesia

64

Figure (3.3) Effects of protocol KT-XY on physiological parameters (respiratory rate, heart rate and


65

Figure (3.4) Effects of protocol KT-XY on physiological parameters (respiratory rate, heart rate and


66

When Thiopentone sodium was used without premedication as elaborated in

Table (5) we observed that, there was non significant (P≥0.05) decrease in the

respiratory rate at time (0 and 10) minutes and non significant (P≥0.05) increase at

time (20, 30, 40, and 50) minutes following induction of anaesthesia. Heart rate

was significantly (P≤0.05) increased all over the duration of anaesthesia course,

while rectal temperature was increased significantly (P≤0.05) immediately after

induction of anaesthesia.

The protocol Thiopentone sodium with diazepam as shown in table (6),

induced significant (P≤0.05) decrease in the respiratory rate which was observed

following induction of anaesthesia at time 10 minutes, then another significant

(P≤0.05) increase at time 50 minutes following induction of anaesthesia was also

observed. The heart rate was significantly (P≤0.05) increased at times (10, 20 and

50) minutes following induction of anaesthesia. Rectal temperature was increased

significantly (P≤0.05) immediately following induction of anaesthesia and a non

significant change was observed at times (10, 20, 30 and 40) minutes.

Injection of Thiopentone sodium with Xylazine as shown in Table (7)

showed that, a significant (P≤0.05) decrease in the respiratory rate was observed at

times (10, 30, 40 and 50) minutes post induction of the anaesthesia. Heart rate

increased significantly (P≤0.05) at times (10, 20 and 30) minutes, while rectal

temperature showed a non significant change.

The combination of Thiopentone sodium with Medetomidine as shown in

table (8) induced a non significant (P≥0.05) decrease in the respiratory rate at times

(0, 10, 40 and 50) minutes following induction of anaesthesia. Heart rate was

decreased significantly (P≤0.05) at times (10, 20, 40 and 50) minutes, while rectal

temperature remained without any significant change until 40 minute.

67

Table (5) Effects of Thiopentone sodium on physiological parameters (respiratory rate, heart rate and rectal

temperature) during the course of anaesthesia

Parameters Time (min)


Respiratory rate 29.0±2.7 23.0±3.6 28.3±2.4 29.3±2.7 31.0±2.9 33.0±2.6 29.6±3.1

(breath/min)

Heart rate 84.0±1.5 100.5±3.9* 95.8±8.1*** 108.8±8.1*** 94.0±5.8** 95.1±5.3** 97.3±4.5**

(beat/min)

Rectal temperature 38.8±0.3 39.1±0.1** 39.0±0.2 39.1±0.2 39.1±0.2 39.2±0.2 39.3±0.2

(°C)

Values are mean ± Standard error of mean of eight replicates each *P ≤ 0.05 **P ≤ 0.001 ***P ≤ 0.0001

68

Table (6) The effects of protocol TH-DI on physiological parameters (respiratory rate, heart rate and rectal



Respiratory rate 28.5±2.1 18.3±4.4 15.5±1.5* 20.0±2.6 24.0±3.5 25.8±3.0 35.1±5.3*

(breath/min)

Heart rate 72.6±3.0 82.8±4.4 85.8±4.5* 86.5±5.6* 83.9±4.3 84.8±6.5 88.0±7.7*

(beat/min)

Rectal temperature 38.81±0.1 39.1±0.2* 39.0±0.2 38.9±0.2 38.8±0.1 38.9±0.2 38.8±0.2

(°C)

Values are mean ± Standard error of mean of eight replicates each *P ≤ 0.05

69

Table (7) The effects of protocol TH-XY on physiological parameters (respiratory rate, heart rate and rectal


Base line value 0 10 20 30 40 50 Respiratory rate 27.3±1.1 8.5±0.9 18.0±5.7*** 13.3±2.1 17.3±3.9** 21.5±4.2** 18.8±3.5** (breath/min) Heart rate 87.0±3.8 105.5±8.5 94.3±9.0* 87.3±10.5* 88.8±10* 86.8±7.6 84.8±7.2 (beat/min) Rectal temperature 38.8±0.3 38.9±0.3 38.7±0.4 38.4±0.4 38.3±0.4 38.1±0.4 37.9±0.5 (°C) Values are mean ± Standard error of mean of eight replicates each *P ≤ 0.05 **P ≤ 0.001 ***P ≤ 0.0001

70

Table (8) The effects of protocol TH-ME on physiological parameters (respiratory rate, heart rate and rectal



Respiratory rate 28.3±0.9 14.5±4.4*** 20.3±2.4 * 20.0±1.6 14.5±1.8 16.5±3.1** 19.0±3.0** (breath/min) Heart rate 84.8±2.2 94.0±4.9 81.8±6.4* 82.0±7.0** 71.3±3.7 74.0±5.4* 73.3±7.3** (beat/min) Rectal temperature 38.8±0.1 39.0±0.1 38.9±0.1 38.7±0.2 38.6±0.2 38.4±0.3 38.4±0.3* (°C)

Values are mean ± Standard error of mean of eight replicates each *P ≤ 0.05 **P ≤ 0.001 ***P ≤ 0.0001

71

Figure (3.5) The effects of Thiopentone sodium on physiological parameters (respiratory rate, heart rate and


72

Figure (3.6) The effects of protocol TH-DI on physiological parameters (respiratory rate, heart rate and


73

Figure (3.7) The effects of protocol TH-XY on physiological parameters (respiratory rate, heart rate and


74

Figure (3.8) The effects of protocol TH-ME on physiological parameters (respiratory rate, heart rate and


75

Following induction of anaesthesia, significant (P≤0.05) decrease was observed at

time 50 minutes.

3.2. Duration of different anaesthetic phases following induction of anaesthesia

with different anaesthetic protocols:

As shown in table (9), the duration of different anaesthetic phases was found

to be as follow:

Generally, Thiopentone sodium containing protocols (TH-DI; TH-XY; TH-

ME) was found to have longer mean periods of anaesthetic phases (25.5±8.9;

29.4±10.3; 30.3±11.2) minutes respectively, when compared to that observed with

Ketamine (5.5±2.7 minutes) or Thiopentone sodium (6.6±6.3 minutes) were used

without premedication. Other protocols were between them KT-XY (18.7±9.2);

KT-ME (18.2±7.0); KT-DI (17.6±3.2) minutes.

The protocol TH-ME was found to have longer time of basal narcosis

(10.7±8.4) minutes, other protocols in descending order were as follows: KT-DI

(6.4±2.8); KT-XY (6.4±2.8); TH-DI (5.5±4.2); KT-ME (4.3±0.6); TH-XY

(4.2±1.6); TH (3.5±4.0); and KT (2.0±0.9) minutes.

The longer mean period of lateral recumbancy phase was reported to be with

the protocol KT-ME with a mean value of (10.1±3.9) minutes. Other protocols

descended as follow: TH-XY; TH-DI; TH-ME; KT-XY; TH; KT-DI; and KT with

mean values of (9.7±4.6; 9.3±6.7; 6.9±5.7; 6.2±3.0; 5.7±9.3; 5.3±2.2; and 1.6±1.0)

minutes respectively.

The descended mean values of sternal recumbancy phase in the different

anaesthetic protocols tested was as follow: (TH-DI; TH-XY; KT-ME; TH-ME; TH;

KT-DI; KT; and KT-XY) and the mean values were (14.9±6.5; 10.0±9.4; 9.7±8.4;

8.9±4.9; 8.8±6.2; 7.6±6.8; 6.1±8.2; and 2.3±2.4) minutes respectively.

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The longer mean value of standing phase was reported to be with the

protocol TH-DI (11.4±7.6) minutes. Other protocols descended as follow: KT+DI;

KT-XY; TH; TH-ME; KT; TH-XY; and KT-ME with mean values of (7.1±6.4;

2.2±4.4; 2.0±2.0; 1.8±2.3; 1.4±0.9; 1.3±1.0; and 1.1±0.9) minutes respectively.

Table (11), shows that there was significant (P≤0.05) increase in total

recovery time (TRT) when premedication was used prior to anaesthesia with

Ketamine or thiopental. Also generally, Thiopentone sodium containing protocols

have significant (P≤0.05) longer duration of TRT than Ketamine containing

protocols.

3.3. Signs observed following injection of selected premedications

When diazepam was injected intravenously into animals, ataxia, star gazing,

salivation, mooning, spontaneous swallowing and sometimes the animal lied into

sternal or lateral recumbancy with the head and neck on the flank.

Following intravenous injection of Xylazine in goats, main signs observed

were aimless wandering, ataxia, salivation, drop of head and tail, rarely star gazing

and sometimes animal lied into sternal recumbancy.

The main sings observed following injection of Medetomidine were smooth

way of adopting sternal recumbancy, salivation and mooning.

3.4. Signs observed following injection of selected anaesthetics

Following injection of Ketamine without premedication, animals roughly

lied down on the ground assuming lateral recumbancy or frog attitude and

sometimes limb paddling. Mooning, nystagmus, dog sitting position and ataxia are

sometimes observed during anaesthesia course.

Thiopentone sodium when injected into animals alone, the animals lied down

on the ground more quiet and sometimes put their heads and neck on the flank

77

region. It’s not uncommon to see paddling, star gazing, and mooning during the

course of anaesthesia.

3.5. Signs observed due to injection of different selected combination

protocols:

The main signs observed in goats following injection of selected

combination of anaesthetics protocols were grunting, snoring, ear and/or head

twitching, paddling with legs, spontaneous swallowing and sometimes chewing

movements. Regurgitation was observed with only two anaesthetic protocols (KT-

DI and TH-ME) and one of the animals died probably due to aspiration of

regurgitated materials, and on post mortem ingesta was found in the trachea and

lungs. Bloat was common with Thiopentone sodium containing protocols. This

adverse effect was solved by sloping head down the body so that saliva and

regurgitated material runs freely from the mouth as suggested by Hall and Clarke

(2001).

3.6. Effect of different selected anaesthetic protocols on reflexes:

Table (10) shows the effects of different selected anaesthetic protocols on

reflexes.

Palpepral reflex was found to be depressed only with anaesthetic protocols

KT-DI, TH-XY, TH-DI, and TH-ME for different periods. Those periods were

found 5.6±1.5; 15.0±4.1; 10.0±4.0 and 8.1±3.1 minutes, respectively. The protocol

TH-XY was found to have longer depression mean time.

KT and TH did not affect tongue reflex. TH-ME (43.8±5.3) minutes seem to

have longer mean time depression of tongue reflex and KT-DI (19.4±3.3) minutes

have shorter one.

Swallowing reflex was not affected with the two protocols KT and TH, but it

was depressed with other selected protocols for different times between TH- XY

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(26.9±4.5) minutes (longer mean time of depression) and KT-DI (5.6±2.6) minutes

(shorter one).

Pedal reflex was not affected with injection of Thiopentone sodium without

premedication, but it was affected with other protocols for different times. TH-ME

(35.6±4.6) minutes seem to have the longer mean depression time of pedal reflex

and KT (6.9±2.4) minutes have the shortest one.

Jaw relaxation reflex was found to be negative during KT and KT-DI

anaesthesia. Other selected anaesthetic protocols were reported to be relaxing jaw

for different periods of time ranging between 40.0±3.8 minutes for TH-XY

representing the longest mean of depression time and 8.8±4.7 minutes for TH the

shortest one.

Most selected anaesthetic protocols were found not to affect the anal reflex

except TH-DI for 15.6±5.5 minutes, TH-XY for 28.8±6.4 minutes, and TH-ME for

33.8±4.9 minutes.

All selected anaesthetic protocols depressed cough reflex for different

periods namely for TH-XY for 42.5±4.5 minutes; KT-XY for 41.3±2.2 minutes;

TH-ME for 36.3±3.7 minutes; KT-ME for 28.8±2.2 minutes; TH-DI for 27.5±5.2

minutes; KT- DI for 20.6±2.4 minutes; KT for 11.3±4.4 minutes; TH for 7.5±2.5

minutes.

3.7. Occurrence of apnoea and regaining of spontaneous respiration due to

Thiopentone sodium

Apnoea was observed when Thiopentone sodium containing protocols were

used. As shown in table (12), the longest duration of apnea was induced with

protocol TH-DI for 75 ± 0.2 seconds, the shortest one was found to be associated

with protocol TH-XY for 44 ± 0.03 seconds, and TH-ME for 56 ± 0.1 seconds

between them.

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Table (9). Duration of different anaesthetic phases after induction of anaesthesia with different selected protocols

Phases

Anaesthetic

Narcosis

Lateral

Sternal

Standing

KT 5.5±2.7 2.0±0.9 1.6±1.0 6.1±8.2 1.4±0.9

KT-DI 17.6±3.2 7.6±2.0 5.3±2.2 7.6±6.8 7.1±6.4

KT-XY 18.7±9.2 6.4±2.8 6.2±3.0 2.3±2.4 2.2±4.4

KT-ME 18.2±7.0 4.3±0.6 10.1±3.9 9.7±8.4 1.1±0.9

TH 6.6±6.3 3.5±4.0 5.7±9.3 8.8±6.2 2.0±2.0

TH-DI 25.5±8.9 5.5±4.2 9.3±6.7 14.9±6.5 11.4±7.6

TH-XY 29.4±10.3 4.2±1.6 9.7±4.6 10.0±9.4 1.3±1.0

TH-ME 30.3±11.2 10.7±8.4 6.9±5.7 8.9±4.9 1.8±2.3

Values are mean (min) ± Standard deviation of mean of eight replicates each

80

Figure (3.9) Comparison of different anaesthetic phases in goats subjected to different anaesthetic protocols

81

Table (10). The effect of different anaesthetic protocols on selected reflexes

Protocols Palpepral Tongue Swallowing Pedal Jaw

relaxationAnal Cough

KT NA NA NA 6.9±2.4 NA NA 11.3±4.4

KT- DI 5.6±1.5 19.4±3.3 5.6±2.6 11.9±4.7 NA NA 20.6±2.4

KT-XY NA 24.4±5.2 17.5±3.6 21.3±2.9 8.8±4.7 NA 41.3±2.2

KT-ME NA 32.5±2.5 21.9±4.1 15.0±5.0 13.8±4.9 NA 28.8±2.2

TH NA NA NA NA 6.9±2.5 NA 7.5±2.5

TH-DI 10.0±4.0 26.3±4.1 12.5±3.1 18.8±2.3 22.5±3.1 15.6±5.5 27.5±5.2

TH-XY 15.0±4.1 41.9±4.6 26.9±4.5 31.9±5.1 40.0±3.8 28.8±6.4 42.5±4.5

TH-ME 8.1±3.1 43.8±5.3 24.4±4.7 35.6±4.6 32.5±5.5 33.8±4.9 36.3±3.7

NA = not affected

Values are mean (min) ± Standard error of mean of eight replicates each

82

Figure (3.10) comparison between the different reflexes tested following application of the different anaesthetic

protocols

83

Table (11) Duration of Total recovery time (TRT) following administration of different anaesthetic protocols

Protocols Mean ± S. E Duncan

Grouping

KT 15.2±3.5 D

KT-DI 41.2±4.2 B

KT-XY 35.3±4.5 B

KT-ME 41.0±2.5 B

TH 26.4±4.2 D

TH-DI 66.2±5.1 A

TH-XY 54.1±5.3 A

TH-ME 56.5±4.4 A Means with the same letter are not significantly different (P>0.05)

Values are mean (min) ± Standard error (S. E) of mean of eight replicates each

84

Figure (3.11) Comparison of total recovery time (TRT) duration in the different anaesthetic protocols.

Time / minutes

85

Table (12) The occurrence of apnea and regaining time of spontaneous respiration associated with protocols

containing thiopental

Protocols

Occurrence of apnoea / Sec

Regaining of spontaneous respiration / Sec

Duration / Sec

TH-DI

16 ± 0.05 91 ± 0.36 75 ± 0.2

TH-XY

20 ± 0.03 64 ± 0.14 44 ± 0.03

TH-ME

17 ± 0.03 73 ± 0.20 56 ± 0.1

Values are mean (Seconds) ± Standard error of mean of eight replicates each

86

Figure (3.12) occurrence of apnoea and regaining of spontaneous respiration following administration of

Thiopentone sodium with the three different premedications

Time/Sec

87

CHAPTER FOUR

88

CHAPTER FOUR

Discussion

With the continuous need for surgical intervention for the treatment and

control of disease conditions in animals; development in anaesthetic techniques

is highly required and indispensible in various animal species.

The current investigation was carried out to compare and contrast the

applicability and safety of application of total intravenous anaesthesia using

number of selected anaesthetic protocols and to provide base line data

concerning intravenous anaesthesia in desert goats. Pre-anaesthetic medications

which are used in this study include two α2-adrenoceptor agonists namely,

Xylazine and Medetomidine, and a benzodiazepine, Diazepam. Anaesthetic

induction agents included Thiopentone sodium and Ketamine Hcl.

Induction agents were used either without premedication or in

combination with one of the three monitored premedications. Selected

physiological parameters, reflexes and anaesthetic phases were measured during

the time course of each anaesthetic protocol. The different anaesthetic protocols

are compared and contrasted and finally graded on the basis of their merits with

regard to their safety and reliability as well as the duration and the type of

recovery.

The significant increase in respiratory rate following induction of

anaesthesia with Ketamine Hcl observed in this study was supported with the

remarks of Hall et al., (2001) who reported that, in clinical practice Ketamine

anaesthesia usually manifested by an increase in respiratory rate. The non

significant changes in heart rate and rectal temperature observed during

Ketamine Hcl anaesthesia in this study is in accordance with the findings of

Dorota et al., (2007) who reported similar results in rabbits.

The protocol Ketamine-diazepam resulted in non significant changes in

respiratory rate, heart rate and rectal temperature, this evidence was in

89

agreement with the findings reported by Ghurashi et al., (2009) in desert goats,

however Muir and Masonen (1982) reported that, this protocol induced

significant increase in respiratory rate in calves.

Monitoring respiratory rate following induction of anaesthesia with the

protocol Ketamine- Xylazine as seen in table (3), induced significant increase

(P≤ 0.05) in respiratory rate at 10 minutes and significant (P≤0.05) decrease at

30 minutes following induction of anaesthesia. Nuha (2004) reported non

significant increase in respiratory rate when used the same protocol in Nubian

goat kids. The significant decrease in respiratory rate observed at 30 minutes in

this study is in the same line with findings of Malik and Singh (2007) in horses.

The non significant increase in respiratory rate was also observed by Muir et al.,

(1977) following administration of Ketamine-Xylazine in horses, and by

Waterman (1983); Blaze, Holland, and Grant (1988) and Kumar et al., (1976) in

domestic goats. According to this study heart rate showed non significant

decrease during Ketamine-Xylazine anaesthesia, this finding is in agreement

with the results obtained by Wixson et al., (1987) in rats. Nuha (2004) in Nubian

goat kids; Muir et al., (1977) in horses; Rings and Muir (1982); and Waterman

(1981) in calves; Colby and Sandford (1982) in cats, reported an immediate

bradycardia at 5 minutes post injection and it persisted for the whole period of

anaesthesia. The non significant bradycardia associated with this anaesthetic

protocol in this study may be due to the Xylazine depressing effect on the

sympathetic activity and its enhancing effects on the vagal activity (Antancio et

al., 1973). The non significant change in rectal temperature associated with

Ketamine-Xylazine supported with the findings of Nuha (2004) and Singh et al.,

(2007). However, Afshar et al., (2005) reported significant decrease in rectal

temperature at time 30 to 60 minutes in goats.

The significant increase in respiratory rate resulted due to administration

of Ketamine-Medetomidine in this study was supported with the findings of Min

90

su, et al., (2004) in rabbits. Nuha (2004) reported a non significant change in

respiratory rate in Nubian goat kids following the usage of the same protocol.

Similar results to those of Nuha (2004) were obtained by Serteyn et al., (1993)

in beagles. However, Moens and Fargetton (1990) reported that the Ketamine-

Medetomidine combination in dogs induced a significant decrease in respiratory

rate and heart rate. While non significant decrease in heart rate and rectal

temperature resulted were in agreement with study of Patricia and Darryl (2002),

who reported similar results. Nuha (2004) and Moens and Fargetton (1990)

reported significant decrease in heart rate and rectal temperature. The drop in

rectal temperature (although non significant) encountered in this study may be

probably attributed to the hypothermic effect of Medetomidine previously

reported in rats by Livingston et al., (1984), Virtanen and MacDonald (1985) or

to the declination of body temperature caused by Ketamine (Beck, 1971).

The non significant decrease in respiratory rate associated with injection

of Thiopentone sodium observed in this study was in agreement with the

findings of Atkinson et al., (1987), Singh and Kumar, (1988) and Taylor,

(1990). However Ghurashi (2008) reported significant increase in respiratory

rate in goat kids due to Thiopentone sodium anaesthesia. This study showed that

heart rate was significantly increased immediately after induction of anaesthesia

with Thiopentone sodium without premedication, this finding is in agreement

with the observations reported by Rawling and Kolata (1983) in goats, Karimi,

(1987) in horses. Although rectal temperature was increased significantly

immediately after induction of anaesthesia with Thiopentone sodium, Kumar

and Sharma, (1986), reported non significant effect of Thiopentone sodium on

rectal temperature in buffaloes.

Monitoring the respiratory rate after induction of anaesthesia with

Thiopentone sodium-Diazepam revealed significant decrease in respiratory rate

and a significant increase at time 50 minute post injection and that agreed with

91

the findings reported by Ghurashi (1999). Significantly increased heart rate was

observed in this study. Rectal temperature was increased significantly

immediately after induction of anaesthesia and non significantly at time (10 – 20

– 30 – 40) minutes post injection of the anaesthetic.

With the protocol Thiopentone sodium-Xylazine there was a significant

decrease in respiratory rate, which started immediately after the injection of the

protocol and continued for up to 50 minutes post induction of anaesthesia. These

results are in accordance with the findings of Rodendo-Garcia et al., (1997) in

dogs and Ghurashi (1999) and Nuha (2004) in goat kids. Prolongation of the

respiratory depressing effect may be due to the use of Xylazine, which was

reported to have a depressing effect on respiration in horses (McCashin and

Gabel, 1975) and in dogs (Vainio and Palmu, 1989). Also there may be some

sort of combined depressing effects on the respiratory rate brought about by

Xylazine and Thiopentone sodium (Thurmon et al., 1996). The significant

increase in heart rate following induction of anaesthesia in this study was in

agreement with finding reported by Ghurashi, (1999) and Nuha, (2004) using

Thiopentone sodium-Xylazine in goat kids. Immediate tachycardia was similarly

reported by using Thiopentone sodium in horses (Karimi, 1987), and in goats

(Contreras and Aspe, 1992). Nuha (2004) reported that the transient tachycardia

continued only for 5 minutes probably because of the bradycardiogenic effect of

Xylazine reported in cattle by Kumar and Sharma (1986). Similar to Ghurashi

(1999) findings, Thiopentone sodium-Xylazine protocol resulted in non

significant decrease in rectal temperature. On the other hand Nuha (2004)

reported significant decrease in rectal temperature starting from 20 minutes post

induction of anaesthesia until full recovery was attained. These results may be

attributed to the fact that Thiopentone sodium depresses the basal metabolism

leading to lowering of body temperature (Hall and Clarke, 1991). Also alpha2-

92

adrenoceptor agonists were reported to cause a dose dependent hypothermia in

rats (Livingston et al., 1984)

Following injection of Thiopentone sodium with Medetomidine,

respiration was non significantly decreased at 0 – 10 – 40 – 50 minutes after

induction of anaesthesia. Heart rate was decreased significantly at 10 – 20 – 40 –

50 minutes post anaesthetic induction. Rectal temperature remained with non

significant changes until 40 minutes after induction of anaesthesia, significant

decrease was observed at time 50 minutes following induction of anaesthesia.

Injection of Diazepam at a dose rate of 0.5mg/kg in goats resulted in

ataxia, salivation and lateral recumbancy, these findings are in accordance with

the observations of Ghurashi et al., (2009) in desert goats. Ataxia was also

reported by Hall et al., (2001). In this investigation, stargazing, mooning and

spontaneous swallowing were also noticed.

In this study, intravenous injection of Xylazine in goats, the main signs

observed were aimless wandering, ataxia which is also reported to occur in

horses (Hall et al., 2001), salivation, lowered head and tail, rarely star gazing

and sometimes animal lied into sternal recumbancy.

The main observations following injection of Medetomidine were smooth

quiet adoption of sternal recumbancy, salivation and mooning.

In this study regurgitation was observed in association with two protocols,

Ketamine - Diazepam and Thiopentone sodium - Medetomidine. Similar

observation was reported by Hall et al., (2001). However, Nuha, (2004) did not

report such observation when used the same protocols in Nubian goat kids

during her experimental work. Although regurgitation of ruminal contents was

generally accepted to represent a serious hazard in ruminants during general

anaesthesia (Hall and Clarke, 1983), it was found that it did not take place in

almost all experimental animals as reported by Ghurashi, (1999) and Nuha,

(2004) in goat kids. That lack of regurgitation could probably attributed to the

93

fact that goat kids rather than adult goats were used in Ghurashi and Nuha

studies. Also Hall and Clarke, (2001) attributed the occurrence of regurgitation

in adult goats to animal positioning particularly lateral recumbancy position.

Also tympany was observed after induction of anaesthesia with different

anaesthetic protocols tested, that is in agreement with findings reported by Nuha

(2004) who observed slight harmless ruminal tympany following induction of

anaesthesia with intravenous anaesthestic agents in Nubian goat kids. This

tympany might be due to the absence of eructation together with occurrence of

salivation (Blood et al., 1994).

Generally, Thiopentone sodium containing protocols (TH-DI; TH-XY;

TH-ME) were found to have longer mean periods of anaesthetic phase

(25.5±8.9; 29.4±10.3 and 30.3±11.2) minutes respectively, compared to that

observed with Ketamine (5.5±2.7 minutes) or Thiopentone sodium (6.6±6.3

minutes) when used without premedication. Other protocols durations were

between the two categories with KT-XY; KT-ME and KT-DI having durations

of 18.7±9.2; 18.2±7.0 and 17.63.2 minutes, respectively.

Induction of anaesthesia with Thiopentone sodium-Xylazine resulted in

anaesthetic phase with significantly longer duration than that obtained when

using Ketamine-Xylazine (Nuha, 2004). This result is supported by the findings

of Kumar et al., (1983) and Kumar and Sharma (1986) who studied the effect of

premedication with Xylazine on Thiopentone sodium anaesthesia in buffaloes.

Similarly these results in this investigation are in agreement with the findings of

Ghurashi (1999), who reported a significant prolongation of anaesthesia phase

when anaesthesia was induced in goat kids with Thiopentone sodium- Xylazine.

The protocol TH-ME was found to have longer duration time of basal

narcosis (10.7±8.4) minutes. Other protocols descended as follow: KT-DI; KT-

XY; TH-DI; KT-ME; TH-XY; TH and KT, with duration time of (6.4±2.8);

(6.4±2.8); (5.5±4.2); (4.3±0.6); (4.2±1.6); (3.5±4.0) and (2.0±0.9) minutes,

94

respectively. Elsewhere the anaesthetic protocol Thiopentone sodium -

Xylazine resulted in a significant prolongation of the narcosis phase when

compared with the other anaesthetic protocols (Nuha, 2004). The prolongation

of the narcosis phase may be due to the profound sedative effect of Xylazine,

which was also reported in goats by Kenaway and Kassen (1994).

The longer mean period of lateral recumbancy phase was noticed with the

protocol KT-ME with a mean value of (10.1±3.9) minutes. Other protocols

descended as follows: TH-XY; TH-DI; TH-ME; KT-XY; TH; KT-DI; and KT

with mean values of (9.7±4.6; 9.3±6.7; 6.9±5.7; 6.2±3.0; 5.7±9.3; 5.3±2.2; and

1.6±1.0) minutes respectively. Significant prolongation of the lateral

recumbancy phase was observed by Nuha (2004), following induction of

anaesthesia with Ketamine-Xylazine when compared with the other anaesthetic

protocols. The significant prolongation of this phase could be mainly attributed

to the administration of Xylazine which was reported to cause a prolonged

lateral recumbancy and profound sedation in man (Vickers et al., 1984) and in

horses (Marroum et al., 1994).

The descended mean values of sternal recumbancy phase with the

different protocols tested (TH-DI; TH-XY; KT-ME; TH-ME; TH; KT-DI; KT;

and KT-XY) was found to be 14.9±6.5; 10.0±9.4; 9.7±8.4; 8.9±4.9; 8.8±6.2;

7.6±6.8; 6.1±8.2; and 2.3±2.4 minutes, respectively.

The longer mean value of standing phase was recorded to be with the

protocol TH-DI (11.4±7.6) minutes. Other protocols descending as follows: KT-

DI; KT-XY; TH; TH-ME; KT; TH-XY; and KT-ME with a mean value of

(7.1±6.4; 2.2±4.4; 2.0±2.0; 1.8±2.3; 1.4±0.9; 1.3±1.0; and 1.1±0.9) minutes

respectively.

The standing time was found to be significantly prolonged following

induction of anaesthesia with Xylazine-Ketamine in goat kids not undergoing

laparotomy when compared with the other tested anaesthetic protocols in

95

animals undergoing laparotomy (Nuha, 2004). This prolongation may be due to

Xylazine injection which was similarly reported to cause difficulty in

maintaining standing position (Vickers et al., 1984).

Table (11), shows that there was significant (P≤0.05) increase in total

recovery time (TRT) when premedications were used prior to the anaesthetic

Ketamine or Thiopentone sodium. Also Thiopentone sodium containing

protocols have a significant (P≤0.05) longer duration of TRT than Ketamine

containing protocols. Induction of anaesthesia with Xylazine - Thiopentone

resulted in a significantly longer duration of total recovery time compared with

the other tested anaesthetic protocols (Nuha, 2004). This prolongation might

probably be attributed to the presence of an additive effect in the combination

used as suggested by Hutch (1976).

Total recovery time is now considered to be among the most important

factors governing the selection of anaesthetic protocols for the various surgical

operations. A lot of surgeons prefer the use of anaesthetic protocols that can

ensure adequate duration of anaesthesia for surgery and as same as time

guarantee a fast, smooth, and uneventful recovery from anaesthesia.

This study suggested that palpepral reflex remained not affected by all

tested protocols, a finding which in accordance with the suggestions of Thurmon

and his colleges (1996), who reported that, the eyes remained open and the

pupils dilated in animals anaesthetized with Ketamine. Palpepral reflex was not

affected with the protocols KT-XY and KT-ME.

Palpepral reflex was affected only with selected anaesthetic protocols KT-

DI, TH-XY, TH-DI, and TH-ME. The protocol TH-XY was found to have

longer depression mean time with a value of 15 minutes.

KT and TH did not affect tongue reflex, TH-ME seems to have longer

mean time of depression of tongue reflex and KT-DI have the shorter depressing

time.

96

Swallowing reflex was not affected with the protocols KT and TH, but it

was depressed with other selected protocols for different time intervals ranging

between TH-ME (longer mean time of depression) and KT-DI (the shorter one).

Pedal reflex was not affected with injection of thiopental without

premedication, but it was affected with other protocols for different duration

times. TH-ME seems to be has longer mean time depression of pedal reflex and

KT has the shorter one.

The regaining time of the pedal reflex, palpeberal reflex, tongue reflex,

jaw reflex, cough reflex and swallowing reflex were monitored during the five

experiments conducted in this investigation where general anaesthesia was used.

The mean regaining time of each reflex was compared with the regaining time

of the same reflex following induction of anaesthesia with the different tested

anaesthetic protocols. The comparison revealed that, the mean regaining time

when using Thiopentone sodium as an induction agent in Xylazine premedicated

animals was significantly longer, probably due the prolongation of the

anaesthesia phase following induction of anaesthesia with Xylazine -

Thiopentone sodium.

All reflexes showed non significant differences in their regaining time

throughout the course of anaesthesia, which was induced using Ketamine Hcl

(Nuha, 2004). This observation may be attributed to the insufficient suppression

of reflexes that was considered to be one of the undesirable effects of Ketamine

(Norwouzian et. al., 1981).

Palpebral reflex was not affected by anaesthetic protocols xylazine-

ketamine and Medetomidine -Ketamine. The reflex persisted throughout the

course of anaesthesia. These results support the findings of Thurmon and his

colleges (1996) who reported that, the eyes usually remain open with the pupils

dilated in animals anaesthetized with Ketamine.

97

Jaw relaxation reflex was found to be negative during KT and KT-DI

anaesthesia, while other selected anaesthetic protocols did affect relaxation of

jaws for different time intervals ranging between those for TH-XY (longer mean

time of depression) and TH (shortest one).

Most selected anaesthetic protocols did not affect the anal reflex except

TH-DI, TH-Y and TH-ME for durations of 15.63, 28.75 and 33.75 minutes,

respectively.

All selected anaesthetic protocols used in this investigation were reported

to depress cough reflex for different periods.

Apnoea is a common finding observed during Thiopentone sodium

anaesthesia, its duration with protocol TH-DI was found to be (75 ± 0.2)

seconds, TH-ME (56 ± 0.1) seconds, and TH-XY (44 ± 0.03) seconds.

98

CONCLUSIONS

AND

RECOMMENDATIONS

99

CONCLUSIONS AND RECOMMENDATIONS

5.1 Conclusions

This study was concentrated on the effects of the two anaesthetic

protocols Ketamine Hcl and Thiopentone sodium with or without premedication

(Diazepam, Xylazine and Medetomidine) in desert goats to provide baseline

data pertaining to different anaesthetic phases tested and to compare it within the

different protocols examined. This study can be concluded as follows:

1. Each of the protocols tested can be used safely in desert goats except

potential hazard of bloat and regurgitation which can be solved by sloping

head down the body so that saliva and regurgitated material runs freely

from the mouth.

2. Usage of premedication prior to Thiopentone sodium and Ketamine Hcl

lead to smooth induction of anaesthesia compared to non premedicated

animals. Physiological parameters (respiratory rate, heart rate and rectal

temperature) were affected to different limits.

3. Usage of premedication prior to Thiopentone sodium and Ketamine Hcl

caused prolongation in total recovery time.

4. Regurgitation was observed with two protocols (KT-DI and TH-ME).

Bloat was common with Thiopentone sodium containing protocols.

5. 5.2 Recommendations

Each of the eight tested protocols at the prescribed dose rates is safe for

use in desert goats, with variable effects on physiological and anaesthetic

parameters. As a future prospect, more investigation is required to be

carried out with other anaesthetic protocols using more sophisticated

monitoring devices.

100

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المستخلص

التـي وريدية ولمخدرات البعض بروتوكوالت االضوء علي ، لقد تقرر تسليط دراسةفي هذه ال

تـوفير هوالدراسة ن هذهالهدف الرئيس م. في السودانإناث الماعز الصحراوي يمكن إستخدامها في

أساسية تتعلق بقياس االطوار التخديرية المختلفة ومقارنتها ببعضها بالعض فـي مختلـف قاعدة بيانات

.البروتوكوالت التي تم اختبارها في هذه الحيوانات

و الماعز الصحراوي الخاليه من االمـراض إناثمن 64 باستخدام عدد التجربةأجريت هذه

تم اسـتخدام كـل مـن عقـار الكيتـامين . متساوية العددمجموعات 8عشوائياً إلي االتي تم تقسيمه

بتركيـز )TH( صـوديوم ونكج من وزن الجسم و عقار ثيوبنت/مج 4بجرعة )KT( هيدروكلوريد

كجم من وزن الجسم تم استخدامهما حقناً بالوريد إلحداث التخدير، كمـا تـم /مج 10وبجرعة % 2.5

)XY( ، الزيالزين مكج/ مج 0.5بجرعة )DI( كعالج تمهيدي هي الديازبام استخدام ثالث عقاقير

اسـتخدمت . مـن وزن الجسـم مكج/ مكج 10بجرعة )ME( و الميديتوميدين مكج/مج 0.1بجرعة

كـل مجموعـة مـن .دقائق من حقن العقـار المخـدر 10عقاقير العالج التمهيدي حقناً بالوريد قبل

مع أو بـدون العـالج ) TH(أو )KT(وره آنفاً تم عالجها إما بإستخدام مجموعات الحيوانات المزك

، KT ،KT-DI ،KT-XY ،KT-ME ،THعليه اصبحت البروتوكوالت هي . التمهيدي

TH-DI ،TH-XY وTH-ME .

قبل إحداث التخدير، و بعد معدل التنفس، معدل ضربات القلب و درجة حرارة الجسمتم قياس

كـل تر المخدرة مباشرة ثم تمت مراقبة الحيوانات أثناء أطوار التخدير و اخذ هذه القراءاحقن العقاقي

كذلك تمت مراقبة المنعكسات االساسيه . دقائق حتى اإلفاقة، باستخدام طرق سريرية قياسية معتمدة 10

.خالل فترة التخدير

أحدث زيادة معنوية في معدل التنفس، KT-ME و KT ،KT-XYاستخدام البروتوكوالت

قـد . إلى انخفاض معنوي في معدل التنفس TH-XY و TH-DIبينما أدى استخدام البروتوكولين

، بينما TH-XY و TH، TH-DIإزداد معدل ضربات القلب معنوياً عند إستخدام البروتوكوالت

حـرارة معنويـاً عنـد إسـتخدام إرتفعت درجة ال. TH-MEانخفض معنوياً عند حقن البروتوكول

، غير أنه لم تهـبط درجـة الحـرارة معنويـاً بإسـتخدام أي مـن TH-DIو THالبروتوكولين

.البروتوكوالت التي تمت دراستها

تحدث أطول فتـرة لطـور التخـدير، TH-MEو TH-DI ،TH-XYوجد أن البروتوكوالت

وتوكـوالت المحتويـة علـى الكيتـامين مقارنة مع ثيوبنتون صوديوم بدون عـالج تمهيـدي و البر

KT، بينما أحدث البروتوكول TH-MEأطول فترة تهويم أساسي تم إحداثها بواسطة . هيدروكلوريد

115

أطول فترة إستلقاء جانبي، بينما اقصر فتـرة KT-MEأظهر البروتوكول . أقصر فترة لهذا الطور

بـأطول فتـرة TH-DIز البروتوكول تمي. KT-DIتمت مالحظتها لهذا الطور كانت عند استخدام

أحـدث البروتوكـول . أظهر اقصر فترة في هذا الطور KT-XYإستلقاء قصي، بيد أن البروتوكول

TH-DI أطول فترة وقوف، غير أن البروتوكولME-KT أظهر اقصر فترة وقـوف مـن بـين

ر و زمـن رجـوع لم تالحظ أي عالقة واضحة بين أطوار التخـدي . البروتوكوالت التي تم إختبارها

.المنعكسات التي تمت مراقبتها

عند إسـتخدام العـالج (TRT) أظهرت هذه الدراسة أن هنالك زيادة معنوية في الزمن الكلي لإلفاقة

التمهيدي قبل الكيتامين هيدروكلوريد أو ثيوبنتون صوديوم، كذلك عموماً البروتوكوالت المحتوية على

ادة معنوية في الزمن الكلي لإلفاقة مقارنة مـع البروتوكـوالت ثيوبنتون صوديوم وجد أنها تحدث زي

. المحتوية على الكيتامين هيدروكلوريد

عند حقن البروتوكوالت المحتوية على ثيوبنتون صوديوم، حيث وجد ) Apnoea(لوحظ توقف التنفس

و أقصـرها بإسـتخدام TH-DIأن أطول فترة توقف للتنفس كانـت عنـد إسـتخدام البروتوكـول

.TH-XYالبروتوكول

خلصت هذه الدراسة إلى أن كل من البروتوكوالت الثمانية التي تم إختبارها حسب الجرع الموضـحة

يمكن إستخدامها بأمان في إناث الماعز الصحراوي، مع مالحظة حدوث آثار متفاوتة على المـدلوالت

.الفسيولوجية و التخديرية

awad hashim bakheit omer - connecting …awad hashim bakheit omer khartoum, june 2009 abstract 15 in...

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