7.2.8.2 after cholecystectomy
TRANSCRIPT
7.2.8.2 After cholecystectomy
Secretin stimulation of doqs with HSV and cholecystectomy signi
ficantly increased the pH of the gastric contents in all of
tnem (Table 37). Raw data is given in Appendix J.
TAB l E 37 : pH OF GASTRIC CONTENTS UNDER BASAL FASTING
CONDITIONS AND DURING SECRETIN STIMULATIC”
IN DOGS WITH HSV AND CHOLECYSTECTOMY
Dog x - SEM
(basal condi
tions )
x - SEM
(secretin
infusion)
Statistical
significance
(t-test)
DD-, 3,539 - 0,078 (13) 4,503 - 0,332 (8) p 0,05
d d 9 3,372 - 0,084 (20) 5,270 - 0,376 (7) p 0,01
DD13
3,430 - 0,254 (21) 5,901 - 0,469 (8) p 0,01
x = mean value of pH
SEM = standard error of the mean
() = numbers ir» parentheses represent the number of tests
7.2.8. 3 Secretin infusion before cholecystectomy
comoared with infusion after cholecystectomy
The pH of gastric contents durinq secretin stimulation in dogs
with HSV and an intact gall bladder was not statistically
different (p 0,05) from the pH during secretin stimulation in
dogs with HSV and a cholecystectony (Table 38)
7.2.3.2 After cholecystectomy
Secretin stimulation of dogs with HSV and cholecystectomy signi
ficantly increased the pH of the gastric contents in all of
them (Table 37). Raw data is given in Appendix J.
TABLE 37 : pH OF GASTRIC CONTENTS UNDER BASAL FASTING
CONDITIONS AND DURING SECRETIN STIMULATION
IN DOGS WITH HSV AND CHOLECYSTECTOMY
Dog x - SEM
(basal condi
tions )
< - SEM
(secretin
infusion)
Statistical
significance
(t-test)
DD? 3,539 t 0,078 (13) 4,503 - 0,332 (8) P 0.05
d d 9 3,372 - 0,084 120) 5,270 - 0,376 (7) P 0,01
DD13
3,430 t 0,254 (21) 5,901 - 0,469 (8) P 0,01
x = mean value of pH
SEM = standard error of the mean
() = numbers in parentheses represent the number of tests
7.2.8.3 Secretin infusion before cholecystectomy
compared with infusion after cholecystectomy
The pH of gastric contents during secretin stimulation in dogs
with HSV and an intact gall bladder was not statistically
different (p 0,05) from the pH during secretin stimulation in
dogs with HSV and a cholecystectomy (Table 38)
TABLE 38 : pH OF GASTRIC CONTENTS DURING SECRETIN
STIMULATION BEFORE AND AFTER CHOLECYSTECTOMY
Dog x - SEM
(secretin before
cholecystectomy)
x - SEM
( s ecretm after
cholecystectomy)
Statistical
significance
(t-test)
DD, 4,109 - 0,35b (7) 4,503 ^ 0,332 (8) p > 0,05
DDg 5,630 ^ 0,456 (8; 5,270 - 0,376 (7) p > 0,05
DD13
5,693 - 0,139 (8) 5,901 - 0,469 (8) p > 0,05
x = mean value of pH
SEM = standard error of the means
O = numbers in parentheses represent the number of tests
7.2.9 Post-mortem findings
7.2.9.,1 Macroscopic f m a m g s
Post-mortem examinations were carried out in all 3 dogs after
they had been sacrificed by intravenous injection of sodium pento
barbitone (section 5.1.3). Besides minor skin sepsis around the
gastrostomy cannula exit site, no other -ibnormality was found.
The stomach, duodenum, liver and spleen were all macroscopically
normal. Nc macroscopic lesions were seen on the gastric mucosa.
210.
7.2.9.2 Histological findings
Control mucosal biopsies were taken from the greater and lesser
curvature of the antrum and fundus, wh^n the HSV was performed
and again at cholecystectomy (section 7.1.10). No mucosal
abnorma’ity was found in any of the biopsies.
After the dogs had been sacrificed, the gastric mucosa was
examined using the ’Swiss r o l l 1 technigue (section 5.1.7).
No abnormal_ty was found in any of the dogs.
211.
7.2.10 Comparison of doqs with HSV with r (a) dogs with
an intact stomach, and (b) dogs with T V + P .
In a previous section, 6.2.15, dogs with IV+P were compared with
dogs with an intact stomach. In this section a comparison will
be made between dogs with HSV (qroup C) and (a) dogs with an
intact stomach (group A), and (fc) dogs with TV+P (group B).
7.2.10.1 Bile reflux under basal fasting conditions
The amount of bile reflux in 3 dogs (25 tests) with HSV was com
pared with the reflux m 5 dogs (35 tests) with intact vagi and
an intact pylorus. There was nc significant difference between
the two groups (Mann-Whitney, p > 0 , 0 5 ) . However, when cholecy
stectomy was added to all dogs, bile reflux was significantly
higher in the group with intact vagi and an intact pylorus (54
tests in group C compared with 71 tests in grcup A, p < 0 , 0 1 ) .
TYie amount of bile reflux in 3 dogs (25 tests) with HSV was com
pared with the reflux in 3 dogs (23 tests) with TV+P and no
significant difference was found (p>0,05). When cholecystectomy
was added to both groups, the dogs with TV+P had significantly
higher reflux than the dogs with HSV (54 tests in dogs of group
C compared with 73 tests in group B, p < 0,01).
7.2.10.2 Bile reflux during secretin stimulation
The amount of bile reflux during secretin stimulation in dogs
with HSV (23 tests) was compared with reflux in dogs with intact
vagi and an intact pylorus (35 tests) and no significant
difference was found (p>0,05). When cholecystectomy was added
to both groups of dogs there was again no significant difference
(23 tests in group C and 43 tests in group A, p>0 , 0 5 ) .
The amount of bile reflux durina secretin stimulation in dogs
with TV+P (30 tests' was significantly higher than in dogs with
HSV (23 tests) (p<0,05). This difference remained so when
cholecystectomy was added to both groups (29 tests in group B
and 23 tests in group C, p < 0 , 0 5 ) .
7.2.10.3 Ratios of lecithin to lysolecithin
7.2.10.3 1 Under basal fasting conditions
The ratios of lecithin to lysolecithin in 3 dogs with HSV (25
tests) were compared with the ratios in 5 dogs with intact vagi
and an intact pylorus (35 tests). In dogs with HSV, the values
of these ratios were significantly higher than in the dogs with
intact vagi and an intact pylorus (p<0,01). When cholecystec
tomy was added to each group, again the ratios of lecithin to
lysolecithin in dogs with HSV (54 tests) were significantly
higher than the ratios in dogs of group A (80 tests) (p<0,01).
The ratios of lecithin to lysolecithin in 3 dogs (25 tests) with
HSV were compared with the ratios in 4 dogs (30 tests' with TV+P.
In dogs with HSV, these ratios were significantly higher (p<0,01)
and remained sc when cholecystectomy was added to both groups
(group E 73 tests, group C 54 tests, p«r. 0,01).
7.2.10.3.2 During secretin stimulation
The ratios of lecithin to ly s o l e c i t h m during secretin stimulation
in dogs with HSV (23 tests) were significantly higher !p<0,01)
than in dogs with m t a c t vagi vid an intact pylorus (35 tests).
This difference remained significant after cholecystectomy was
performed on both groups of dogs (36 tests in group A, 23 in
group C, p <0,01).
The ratios of lecithin to l y s o l ecithm during secretin stimula
tion in dogs with HSV (23 tests) were significantly higher
(p<9,01) than in dogs with TV+P .and secretin stimulation (30
tests). This difference remained significant after cholecystec
tomy was added to both groups (30 tests in group B and 23 m
group C, p < 0,01).
7.2.10.4 Volumes of gastric contents
7.2.10.4.1 Under basal fasting conditions
The pre-cholecystectomy volumes of gastric contents collected
under basal fasting conditions in dogs with HSV (25 tests) were
significantly smaller (p<0,01) than in dogs with lr.tact vagi
and an intact pylorus (35 tests). This difference remained
significant after a cholecystectomy was added to both groups
(80 tests in group A, 54 in group C, p < 0 , 0 1 ) .
The pre-cholecystectomy volumes of gastric contents in dogs with
HSV (25 tests) were significantly smaller (p<0,01) than in dogs
with TV+P (30 tests). After a cholecystectomy was added to both
groups, this difference remained significant. (73 tests in group
B, 54 in group C, p<0 , 0 1 ) .
7.2.10.4.2 During secretin stimulation
The pre-cholecystectomy volumes of gastric contents during
secretin stimulation in dogs with HSV (23 tests) were signifi
cantly smaller (p<0,01) than in dogs with intact vagi and an
intact pylorus (35 tests). After cholecystectomy was performed
on both groups of dogs, secretin stimulation in dogs with HSV
(23 tests) was igain associated with smaller volumes (p<0,01)
than those in dogs of group A (36 tests).
The pre-choiecystectomy volumes of gastric contents during
secretin stimulation in dogs with HSV (23 tests) were signifi
cantly smaller (p<0,01) than in dogs with TV+P (30 secretin
tests). This difference remained significant after cholecystec
tomy was carried out on all dogs (29 secretin tests in group B,
23 in group C, p < 0,01).
7.2.10.5.1 Under basal fasting conditions
The pre-cholecystectomy pi! of gastric contents in dogr with HSV
(25 tests) was significantly higher (p<0,01) than m dogs with
intact vagi and an intact pylorus (35 tests). This difference
remained significant after cholecystectomy was performed on all
dogs (80 tests in group A, 54 in group C, p<0 , 0 1 ) .
The pre-cholecystectomy pH of gastric contents in dogs with HSV
(25 tests) was net significantly different from the pH in dogs
with TV+P (30 tests, p > 0 , 0 5 ) . The pH in dogs with TV+P post
cholecystectomy (73 tests) was significantly higher (p<0,05)
than that m dogs with HSV (54 tests).
7.2.10.5.2 During secretin stimulation
The pre-cholecystectomy pH iurinq secretin stimulation in dogs
with HSV (23 tests) was significantly higher (p<0,01) than
that in dogs with m t a c c vagi and an intact pylor’is (35 tests).
This difference remained significant after a cholecystectomy
was added to all dogs (23 secretin tests in group C and 43 in
group A ).
The pre-cholecvstectomy pH during secretin stimulation in dogs
with HSV (23 tests) was significantly lower (p<0,01) than in
dogs with TV+P (30 secretin tests). This difference remained
unchanged after cholecystectomy (23 secretin tests in group C
7.2.10.5 pH of gastric contents
and 30 in group B, p < 0 , 0 1 ) .
7.2.10.6 Histological findings
None of the doas with HSV developed any mucosal abnormality,
whilst 2 of the 5 dogs with an intact stomach and 2 of the 4
dogs with TV+P develoDed gastritis by the end of the experiments.
7.3 DISCUSSION
7.3.1 Discussion of materials and methods
In this part of the study, 4 dogs were used. One of then ( D D ^ )
was excluded due to a positive Hollander test, therefore tests
were performed on only 3 dogs. While the number of dogs used
was relatively small, each dog acted as its own control and a
large number of tests were carried out on each animal. A total
of 79 tests on the 3 animals were carried out under basal
fasting conditions, and 46 during secretin stimulation.
7.3.2 Discussion of biochemical findings
The amount of bile reflux in the 3 dogs with HSV did not differ
significantly from the reflux that occurred in the 5 dogs in
group A (intact vagi and an intact, pylorus) nor from that which
was seen in 3 of the 4 dogs of group B (TV+P) (section
7.2.10.1;. However, the nature of the refluxed bile was
different: the ratios of lecithin to lysolecithin in dogs with
TV+P or HSV were significantly higher than in dogs with intact
vagi (section 7.2.10.3.1). It may be that vagotomy inhibits
the production of l y s o l e c i t h m from lecithin. In the case of
TV+P the possible mechanisms have been discussed in section
6.3.1. A possible explanation of the effect of HSV on lysoleci-
t h m production is that HSV may indirectly inhibit secretin
release by inhibiting gastric acid secretion. It is known that
hydrochloric acid stimulates the release of s e c r e t m (81). In
the present study, s e c r e t m was found to prom te lysolecithm
production.
When cholecystectomy was performed on all dogs with HSV, reflux
did not increase. In contrast with this observation, reflux did
increase in choiecystectomized dogs with TV+P or with m t a c t
vagi (sections 5.2.6 and 6.2.6). It seems that HSV prevents D/G
reflux. Dewar et al (245,247,266) reported that the concentra
tion of bile acids and lysolecithm m the stomach of patients
with gastric or duodenal ulcers decreased significantly after
a HSV was performed. The authors suggested that after HSV, the
receptive relaxation of the gastric fundus was lost, resulting
In increased m tragastr ic pressures. These high pressures com
bined with an intact antropyloroduoden.il segment may prevent
reflux from the duodenum into the stomach. Furthermore, the
increased rate of ga.stric emptying of liquids which follows HSV
might discourage reflux. An alternative explanation in human
patients with duodenal ulcer may be that HSV allowed the ulcer
to heal, so that a normal physiological state was restored.
Results in the present study suggest that HSV is associated
with faster emptying of liouids than occurs with TV+P: the
volumes of gastric contents in dogs with HSV were significantly
smaller than in dogs with TV+P (section 7.2.10.4.1). Ihe
volume of gastric contents in a fasting state are determined
mainly by three factors: gastric secretion, gastric emptying,
and duodeno-gastric reflux. It is unlikely that the rate of
gastric secretion was different .n dogs with HSV or TV, since
in both groups the same acid secreting areas were denervated.
Duodeno-gastric reflux would be expected to be the same in both
groups since all the dogs with HSV and 3 dogs with TV+P had the
same concentrations of lecithin ind lysolecithin in the stomach
If the gastric secretion rate and D/G reflux can be disregarded
the most probable cause of smaller volumes of gastric contents
in dogs with HSV, is a faster gastric emptying of liquids. If
this is so it could be an expla’ jn as to why cholecystectomy
combined with HSV was not associated with increased bile reflux
a fast gastric emptying of liquids may discourage D/G reflux
and empty any refluxed material before it mixes with gastric
contents. However this hypothesis is presented with reserva
tions since previous studies have not shown a faster emptying
of liquids in HSV than TV+P. A detailed review of the relevant
literature is presented in section 3.1.2.3.
Secretin stimulation in dogs with HSV promoted bile reflux into
the stomach, both before .and after cholecystectomy. A possible
explanation might be the effect of secretin on the pressure
gradient across the pylorus. A detailed discussion has been
presented in section 5.3.2.
As in dogs of groups A -»nd B, secretin favoured lysolecithin
production both ocfore and after cholecystectomy. Possible
explanations have been given in section 5.3.2.
Secretin stimulation m dogs with HSV resulted ir significantly
lesser amounts of bile reflux than in dogs with TV+P, both before
.ana after cholecystectomy (section 7.2.10.2). It seems that the
pressure changes induced by secretin at the antroduodenal region
and the oresence of pyloroplasty make local conditions more
favourable fcr reflux.
7.3.3 Clinical s ignificance of the results of the
present study
The results of the present study suggest that HSV might protect
the stomach against D/G reflux in two ways: firstly by dis
couraging D/G reflux and secondly by inhibiting production of
lysolecithin from lecithin. Pathophysioiogically, lysolecithin
is a cytotoxic agent which damages gastric mucosa. The present
experiments showed that when cholecystectomy was added to HSV
there was no increased reflux as was the case in cholecystecto-
rr.ized dogs with intact vagi or with TV+P. Dewar et al (245,
(247, 266) showed that HSV decreased bile reflux in humans with
gastric or duodenal ulcers. However, it still remains tc be
shown if increased bile reflux in the absence of peptic ulcer
will reverse after HSV. This could be studied by performing an
HSV on dogs with increased bile reflux after cholecystectomy.
However this was not undertaken in the present study because of
the technical difficulties associated with HSV in the presence
of a permanent gastrostomy cannula. This matter will be the
subject of a future study.
7.4 CONCLUSION
The object of this parr of the present investigation was to
examine the relationship between bile reflux into the stomach
srd cholecystectomy under different experimental conditions.
The amount of bile reflux in dogs with HSV before and after
cholecystectomy, and after secretin stimulation was measured.
HSV alone was associated with the same amount of bile reflux
that occurred both in dogs with intact vagi, and in most of the
animals who had undergone TV+P.
When a cholecystectomy was added to the HSV, reflux did not
increase. However, when a cholecystectomy was carried out in
dogs with intact vagi and an intact pylorus (group A) or in
dogs with TV+P (group E), there was a significant increase in
the amount of bile reflux. A possible explanation for the post-
221.
cholecystectomy increased bile reflux in groups A .and B has been
offered in sections 5.3.2 and 6.3.1.
A possible explanation as to why HSV combined with cholecystec
tomy was not associated with increased reflux, is that the
increased i ntragastnc pressures which follow HSV, combined with
an intact antropyloroduodenal segment, might discourage reflux.
A more rapid gastric emptying following HSV may clear any
refluxed bile from the stomach rapidly, and thus prevents it
from mixing with g e s t n c contents. The mucosa would therefore
be exposed to the effect of bile for a period that would be
insufficient to allow damage to occur. In addition, HSV7 may
inhibit the production of lysolecithin, a substance known to be
cytotoxic, and possibly of importance in the pathogenesis of
gastritis.
Under the experimental conditions described, it was established
that an increase of bile reflux into the stomach follows chole
cystectomy in dogs with an intact stomach or TV+P. However,
cholecystectomy' in dogs with HSV did not increase bile reflux.
While again the Janger of extrapolation from tho animal to the
human situation is well recognized, it would seem that should a
human subject require surgical management for combined ducdenal
ulceration and gall bladder disease at the same time, cholecy
stectomy and HSV would be the appropriate procedures.
FINAL CONCLUSION
-r- .
■/ '
223,
An experimental study was designed tc investigate the possible
relationship between cholecystectomy and the occurrence of bile
reflux into the stomach, under various conditions. Duodeno-
g a s t n c reflux is an intermittent phenomenon which varies from
time to time in the same experimental animal. In order to
obtain a meaningful assessment of reflux, a large number of
experiments, over long periods of time, were performed on each
dog. Cholecystectomy alone was found to promote bile reflux
into the stomach. This is probably the result of the continuous
presence of bile in the duodenal contents which fo]lows cholecy
stectomy. However, in 2 cf the 5 dogs the post-cholecystectcmy
increase of the amount of bile reflux was transient, lasting for
ebout 2 months, and then returning to pre-cholecystectomy levels.
This could be the result of changes of the common bile duct,
which, in dogs, dilates after cholecystectomy. A dilated common
bile duct may take over part of the reservoir function cf the
gall bladder. Two of the dogs with consistently increased post-
cholecystectcmy bile reflux developed histological gastritis.
TV+P alone was not invariably associated with increased bile
reflux. However, when cholecystectomy was added, all docs
developed persistently increased .amounts of bile reflux. This
reflux was not significantly higher than that observed m dogs
with cholecystectomy alone. These results suggest that perhaps
the pylorus does not play a major role in preventing duoceno-
8. FINAL CONCLUSION
*
gastric reflux. Two of the dcqs with.TV+P and cho"ecystectomy
developed histological gastritis, 6 months after cholecystectomy,
when the study was concluded.
HSV alone was associated with the same amount cf bile reflux as
was observed in dogs with an intact stomach, and in 3 of the 4
dogs with TV+P. However, when cholecystectomy was added there
was no increase in reflux. It is possible that HSV may dis
courage reflux. Alternatively, any refluxed material may empty
faster before mixing with gastric contents. None of the dogs
with HSV developed histological gastritis.
Both HSV and TV+P seem to inhibit the production of lysolecithin
from lecithin. Pathophysiologically, this is important because
lysolecithin is a cytotoxic agent which is injurious to gastric
mucosa. Secretin stimulation promoted d u o d enogastnc reflux in
all groups of dogs, probably by changing the pressures in the
antropvloroduodenal segment. Secretin promoted lysolecithin
production in all groups cf dogs.
While recognizing the danger cf extrapolation of experimental
results to humans, it would seem from this experimental study
that some cases of the so-called 'post-cholecvstectomy syndrome'
might be due to abnormal amounts of bile refluxing into the
stomach. The results of the present study suggest that the
amount cf reflux that, occurs with TV+P and cholecystectomy, is
not more than that which occurs with cholecystectomy alone.
Moreover, reflux with HSV and cholecystectomy is less than the
reflux observed with cholecystectome alone, or with TV+P and
cholecystectomy.
REFERENCES
1. , Beaumont, W. Experiments and Observations on the Gastric
Juice and the Physiology of Digestion. 2nd Edition.
New York: Dover, 1833.
2. Boldyreff, W. The self-regulation of the acidity of the
gastric juice. Quart J. ex. Physiol., 7: 1-12, 1914.
3. Hicks, C. and Visher, J.W. Contributions to the physio-
loqy of the stomach. The mechanism of regurgitation of
duodenal content.1- into the stomach. .'Vn. J. Physic 1.,
39: 1-8, 1915.
4. Sp.'ncer, W.H. et a l . Gastrointestinal studies. Direct
evidence of duodenal regurgitation and its influence
upon the chemistry and function of the normal human
stomach. Am. J. Physiol., 39: 459-479, 1916.
5. MacLean, H. and Griffiths, W.J. The factors influencing
the concentration of hydrochloric acid during gastric
digestion. J . Fhysiol. (Lond .), 65: 63-76, 1928.
6. Grant, R. The cytolytic action of some gastro
intestinal secretions and enzymes on epithelial cells of
the gastric and duodenal mucosa. J. cell. comp. Physiol.,
37: 137-161, 1951.
7. Palmer, E.D. Gastritis: a revaluation. Medicine,
Baltimore. 33: 199-200, 1954.
8. Du Plessis, D.J. Gastric mucosal changes after resection
of the stomach. S. Afr. Med. J . 36: 4 71-478, 1952.
9. Du Plessis, D.J. Pathogenesis and surgical management of
peptic ulcer. S. A f r . M e d . J ., 34: 101-108, 1960.
10. Du Plessis, D.J. The importance of the pyloric antrum in
peptic ulceration. 5. A f r . J . Surg., 1: 3-11, 1963.
11. Lawson, H.H. Effect of duodenal contents on the gastric
mucosa under experimental conditions. Lancet^, 1: 469-472.1964
12. Mosimann, F., Burri, B., Diserens, H. et al. Elitero-
g a s t n c reflux: Experimental and clinical study.
Sca n d . J. Gastroent, 16: 149-152, 1981.
13. Fehr, H.E., Aebi, M., Finger, J. and Clemenson, G.H.
Inhibition of exoerimental stress ulcer formation in rats.
Scan. J. Gastroent., 16: 187-189, 1981.
Cheli, R., riacosa, A. and Molinari, F. Chronic atrophic
gastritis and duodenogastric reflux. Scand. J. Gastroent.
16: 125-127, 1981.
Rhodes, J. The clini ' significance of bile reflux.
Scand. J . Gastroent., 173-175, 1981.
Menguy, R., Max, M.H. Influence of bile on the canine
gastric-antral mucosa. A m . J . S u r g ., 119: 177-182, 1970.
Bedi, B.S., Debas, H.T., Gillespie, G., et a l . Effect of
bile salts on antral gastrin release. Gastroenteroloav,
60: 256-262, 1971.
Capper, W.M., Butler, T.J , Buckler, F.G. Alkaline areas
in gastric mucosa after gastric surgery. Gut 7: 220-222,
1966.
Delaney, J.P., Broadle, T.A., Robbins, P.L. Pyloric reflux
gastritis: The offending agent. Surgery, 77: 764-772, 1975.
Braun, S.A., Samson,R.H.. Norton, L. Bile reflux in
experimental stress ulcer. Surgery, 73: 521-524, 1973.
Mann, N.S. Bile-induced acute erosive gastritis. Dig. D i s .
21: 89-92, 1976.
Yokoyaina, M., Tatsuta, M. , Baba, M . f et al. Bile reflux:
A possible cause of stomach ulcer in non-treated mutant
mice of W/W genotype. Gastroenterology, 82: 857-863, 1982.
Lawson, H.H. The production of chronic gastritis under
experimental conditions. Scand. J. Gastroent., 16: 91-98,
1981.
Clemenson, G.H., Finger, J. and Fehz, H.F. The role of
taurocholic acid, glycocholic acid and lysolecithin in
experimental stress ulcer in the rat. Scand. J. Gastroent.,
16: 137-140, 1981.
Johnson, A.G., McDermott, S.J. Lysolecithin: A factor
in the pathogenesis of gastric ulccration? Gut., 15: 710-
7.13, 1974.
Davenport, H.W. Effect of lysolecithin, digitonin and
phospho1ipase A upon the dcg's gastric mucosal barrier.
Gas t roen tero1o g y , 59: 505-509, 1970.
Kivilaasko, E., Ehnholm, C., Kalima, T.V. et al.
Duodenogastric reflux of lysolecithin in the pathogenesis
of experimental porcine stress ulceration. Surgery, 79:
65-69, 1976.
Johnson, A.G. Lysolecithin: A factor in the pathogenesis
of gastric ulceration? G u t , 13: 843 , 1972.
Clemencon, G., Noctural m tragastr ic pH measurements.
Scand. J . Gastroent., 7: 294-298, 1972.
Keane, F.B., Dimsngo, E.F., Malagelada, J.R. Du<xieno-
gastric reflux in humans: Its relationship to fastxng
antroduodenal motility and gastric, pancreatic and
biliary secretion. Gistroentero1o g v , 81: 726-731, 1981.
Munk, J .F ., Johnsor, A .F . Effect of Duodenal and Antral
Picinq on Pyloric Reflu> in the C a t . Gastrointestinal
MOtility, New York: Raven press, 1980, 173-175.
Stemper, T.J., Cooke, A.R. Effect of a fixed pyloric
opening on gastric emptying in the cat and dog.
Am. J. Physiol., 230: 813-817, 1976.
Rovelstad, R.A. The m e mpetent pyloric sphincter.
Dig. Pis., 21: 165-173, 1976.
Brooks, W.S., Wenger, J., Hersh, T. Bile reflux gastritis.
.Am. J. Gastroent. 64: 286-292, 1975.
Wormsley, K.G. Aspects of duode.no-aastnc reflux in man.
Guc, 13: 243-250, 1972.
Lipshutz, W., Cohen, S. InteriCtion of gastrin I and
secretin on gastrointestinal circular muscle. Am. J.
Physiol., 222: 775-781, 1972.
Fisher, F.S., Cohen, S. Pyloric sphincter dysfunction in
patients with gastric ulc^r. N. Enal. J. ’led. 288: 273-
276, 1973.
Rock, E.#> Malmud, L - , Fisher,R.S. Motor disorders of the
stomach. Med. Clin. North. 'm., 6: 1269-1289, 1981.
Menguy, P.B., Hallenbeck, G.A., Bollman, J.L., et al.
Intraductal pressures and s p h i n c t e n c resistance in canine
pancreatic and t liary ducts after various stimuli.
Surg. Qyn. Ob.it., 100: 306-319, 1958.
Sonnenberg, A., L.issner, S. A.M., Schattermann, G., et a l .
A quantitative assessment of duodenogastric reflux in the
dog after meals and under pharmacological stimulation.
Scand. J. Gastroent., 16: 103-105, 1981.
Kalima, T . , Sjoberg, J. Bile reflux after cholecystec
tomy. Scand . J . G.»r.t r.'ont ., 67: 153-i56, 1981.
Johnson, A.G. cholecystectomy and gall stone dyspepsia.
Ann . R o y . Col1. Surg. E n g ., 56: 69-80, 1975.
Taylor, T.V., Lambert, M.E., Qureshi, S. et al. Should
cholecystectomy be combined with vagotomy and pyloro
plasty? Lancet, 1: 295-298, 1978.
Warshaw, A.L. Bile gastritis without prior gastric
surgerv: contributing role of cholecystectomy. Am.J. Surg.
137: 527-531, 1979.
MacKie, C.R., Wisbey, M., Cuschieri, A. M i l k ^ T c m -£HIDA
test for enterogastric bile reflux. Br. J. Sura. 69:
101-104, 1982.
Capper, W.V., Butler, T.J., Kirby, J.O. et al. Gall
stones, gastric secretion, and flatulent dyspepsia.
Lancet. 1: 413-415, 1976.
Earlam, R. Bile re'lux and the Roux en Y anastomosis.
Er. J. Sura., 70: 39;-397, 1983.
— , — .... — -............■- ' *
Ear lam, R., Thomas, M. Th<- >cal significance of gall
stones ard their radiologit . ^stigation. Br. J. Surg.
65: 164-167, 1978.
Lee, S.P. The st^r ch after cholecvstactomy. Am. J. Surg.
146: 325-327, 198
Brink, B.V., Schlegel, J.F., Code, C.F. The pressure
profile ot the gastro-duodenal junctional zone in the
docs. Or_, 6: 163-171, 1965.
Edwards, D.A.W. Physiological concepts of the pylorus.
Pr o c . Roy. S o c . Med. 54: 930-933, 1961.
Daniel, E.E., Carlow, D.R., Wachter, B.T., et a l .
Electrical activity of the small intestine. Gastro-
enterology, 37: 268-281, 1959.
Alvarez, W.C. An Introduction to Gastroenterology. 4th
Edition. New York: Paul E. Hoeber, Inc., 1940.
Braithwaite, L.R. The role of b:le in duodenal regurgita
tion. B r . J . Surg., 31: 3-13, 1943.
Kelly, K.A. Gastric motility after gastric operations.
S u r g . Ann. 6: 103-123, 1974.
Daniel, E.E., Irwin, J. Electrical Activicy of Gastric
Musculature. Handbook of Physiology. Section 6:
Alimentary canal. Code, C.F., Heide!, W. (eds.)
Washington, HC: 1968.
c>-
Eiwards, D.A.W., Rowlands, E.N. Physiology of the Gastro
duodenal Junction. Handbook of Physiology. Cede, C.F.,
Heidel, W. (eds.), Washington, DC, 1968.
Eedi, B.S., Code, C.F. A study of pathways for the c o
ordination between myoelectric activities of the antrum
and duodenum. Br.J. Surg., 59: 305-3D6, 1972.
Brooks, F.P. Gas *• r ; i nt er t i r. a 1 pa t he rhy.-: : o l'<r/ . New York:
University Press, 1974.
Code, C.F. Discussion at the Symposium of Gastrointestinal
Research, Roche.--ter, Minnesota. Mayo Foundation. February
21 and 22, 1975.
Kelly, F.A., Schlegel, J.F., Code, C.F. Duodenal-gastric
reflux caused by retrocrade duodenal pacing. Mayo Clin.
Proc., 50: 534 * , 1975.
Mehta, S.J., Kaye, M.D., Showalter, J.P. Is there a
pyloric sphincter? (Abstract). Gastroenterology 66: 746
1974 .
Anderson, S., Grossman, M.I. Profile of pH, pressure and
potential difference at gastroduodenal junction in man.
Gastroenterology, 49: 364-371, 1965.
Kaye, M.D., Showalter, J.P. Pyloric incompetence in patients
with symptomatic gastroesophageal reflux. J. Lab. Clin. Med.,
3: 196-206. 1974.
Torgerson, J. The muscular build and movements of the
stomach and duodenal bulb. Acta Radiol. (Suppi.) 45: 182
1942.
Fisher, R., Cohen, S. Physiological characteristics of the
human pyloric sphincter. Gastroenterology S 4 : 67-75, 1973.
Fisher, R.S., Lipschutz, W„, Coher.,S. The hormonal regula-
lation of pyloric s o h m c t e r function. J. Clin. Invest. 52:
289-1296, 1973.
Ar.uras, S., Cooke, A.P., Christense, J. Ar, inhibitory
innervation at the gastro-duodenal junction. (.Abstract1
Gastroenteroloav, 66: 660, 1974.
-■r-i ’ •
Rothmund, M., Grimm, W., Ee.nken, U. Experimentelle Unter-
suchungen zum E m f l u b der pyloroplastik auf magenentleerung,
Sezumgastrin und duodenogastnschen reflux bei selektiv
proximaler vagotomie (English abstract). Chirura, 49: 574,
1978.
Gleysteer., J.J., Wood, M.D., Burdens haw, J.A. et a l .
Ga.- ric e m p f i r o -f .li'uid. after different vagotomies and
py ; i-lasty". 5. C - ■ •. ?fc.--~e* . . 142: 41-43, 1976.
251
71,
72,
73,
74.
75,
76.
Idem. Gastric emptying following Finney pyloroplasty and
vagotomy. Am. J . D i g . P i s . 15: 347-350, 1570.
Kilby, J.O. Duodenogastric reflux and pyloric surgery.
Brit. J. Surg., 3: 235, 1972.
Sonnenberg, A., Lepsien, G., Schattenmann, G., et al.
Duodenogastric reflux in the dog following pharmacological
antral and pyloric inhibition. (Abstract). Proceedings
of the 7th International Symposium on Gastrointestinal
Motility, Iowa City, Iowa. 1979: 38.
Munk, J.F., Johnson, A.G. Effect of duodenal and antral
pacing on pyloric reflux m the c a t . (Abstract).
Proceedings of the 7th International Symposium on Gastro
intestinal Motility, Iowa City, Iowa, 1979: 40.
Sonnenberg, A., Schattenmann, G., Lepsien, G., et a l .
The determinants of duodeno-gastric reflux - A quantitative
meausrement in the dog. Gastrointestinal Motility. Raven
Press, New York, 169-172, 1980.
Davidson, E.D., Hersh, T. Bile reflux gastritis.
A m . J . S u r g ., 130: 514-518, 1975.
Hunt, J.N., Ramsbottom, N. Effect of gastrin II on gastric
emptying and secretion during a test meal. Br. Med. J. 4:
386-387. 1967.
78, Geller, L.I., Petrenko, v’.F. Effect of secretin and pan
creozymin on intracavitary pressure in the stomach and
duodenum, evacuation from the stomach, and the tone of
: . ric sphincter. Human Physi^i. 6: 64-48, 1980.
79. Hacki, K.H. Secretin. Clin, in Gastroent.
1980.
: 609-632,
80.
81,
82,
8 3 ,
84
Chrasta, T.E., Cooke, A.R. Secretm-gastric emptying and
motor activity: Natural versus synthetic secretin.
Proc. S o c . Exp. Biol. M e d . 142: 137-142, 1973.
Hubei, K.A. Secretin: A long progress note. Gastro
enterology . 62: 318r339, 1972.
Vange, M., Andre, C. The effect of secretin on gastric
emptying in man. Gastroenterology. 60: 421-424, 1971.
Chey, W.Y., Hitanant, S., Hendricks, J. Effect of secretin
and cholecystokinin on gastric secretion in man. Gastro
enterology, 58: 820-827, 1970.
Capper, W.M. Factors in the pathogenesis of gastric ulcer.
Ann. R o y . Co11. Surg. E n g . 40: 21-35, 1967.
«
Crider, J.O., Thomas, J.E. A study of gastric emptying
with the pylorus open. Am. J. Dig. D i s . Nutr. 4: 295-
300, 1937.
Keet, A.D. The prepyloric contractions in the normal
stomach. Acta Radiol. (Stockh.) 48:4-13-424, 1957.
Williams, I. Closure of the pylorus. B r . J. Radiol.
35: 653-670, 1962. ‘
Lawaetz, 0., Olesen, H.P., Wandall, H.H. Effect of
truncal vagotomy and pylorotomy on gastric emptying.
Scand. J. Gastroent. 17: 825-831, 1982.
Cobb, J.S., Bank, S., Marks. I.N. Gastric emptying after
vagotomy and pyloroplasty. Dig. Pis. 16: 207-215, 1971.
Faxen, A., Berger, T., Kewenter, J., Kock, N.G. Gastric
emptying after different- surgical procedures for duodenal
ulcer. Scand. J. Gas tr per, t . 12: 983-987( 1977.
Wastel, C., MacNaughtcn, J.I., Collin, J.F., Gleeson, J.
Gastric secretion and emptying before and after parietal
cell vagotomy, with and without pyloroplasty.
B r . J . Surg. 58: 871, 1971.
Wilbur, B.G., Kelly, K.A. The effect of gastric fundec-
tomy on canine gastric pacesetter potential, transmural
pressure, and emptving. (Abstract). Gastroenterology.
62: 863, 1972.
Nelsen, T.S., Kohatsu, S. The stomach as a pump.
Rend. Ro m a . Gastroent. 3: 65, l ^ i .
Wilbur, G.G., Kelly, K.A. Effect of proximal gastric,
complete gastric, and truncal vagotomy on canine gastric
electric activity, motility, and emptving. Ann. Surg.
178: 295-303, 1973.
Stadaas, J., Anne, S. Intragastrie pressure/volume
relationship before and after vagotomy. Acta O u r Scand.
136: 611-615, 1970.
Koster, N . , Madsen, P. The intragastrie pressure before
and immediately after truncal vagotomy. Scand. J .
Gastroent. . 5: 381-386, 1970.
Jahnberg, T., Martisnon, J., Hulten, L., Fasth, S.
Dynamic response to expansion before and after vagotomy.
Scand. ,1. -vn; . 10: 593-598, 1975.
Berger, C.L., Hamfelt, A., Meurlmg, S. Effect of highly
selective vagotomy on gastric emptying. Scand. J .
Ggstroenj . 11: 829-832, 1976.
Author Demetriades D Name of thesis The effect of cholecystectomy on duodenogastric reflux an experimental study 1984
PUBLISHER: University of the Witwatersrand, Johannesburg
©2013
LEGAL NOTICES:
Copyright Notice: All materials on the Un i ve r s i t y o f the Wi twa te r s rand , Johannesbu rg L ib ra ry website are protected by South African copyright law and may not be distributed, transmitted, displayed, or otherwise published in any format, without the prior written permission of the copyright owner.
Disclaimer and Terms of Use: Provided that you maintain all copyright and other notices contained therein, you may download material (one machine readable copy and one print copy per page) for your personal and/or educational non-commercial use only.
The University of the Witwatersrand, Johannesburg, is not responsible for any errors or omissions and excludes any and all liability for any errors in or omissions from the information on the Library website.