plantilla programa ciencia. glaucomoa

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GLAUCOMA: Neuroprotección

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Fisiología

Atlas de oBalmología clínica del perro y el gato. Ed Sevet 2007

Fisiología No se puede mostrar la imagen. Puede que su equipo no tenga suficiente memoria para abrir la imagen o que ésta esté dañada. Reinicie el equipo y, a continuación, abra el archivo de nuevo. Si sigue apareciendo la x roja, puede que tenga que borrar la imagen e insertarla de nuevo.

Topics in Companion Animal Medicine 2008, 23(1)

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Fisiología THE GLAUCOMAS ! 231

Balancing Aqueous Production and Outflow

IOP is the result of a delicate balance between production andoutflow of aqueous humor (Figure 12-3). In glaucoma bothproduction and outflow are altered. Usually a large percentageof the outflow pathway (perhaps as much as 80% to 90%)needs to be impaired before IOP starts to rise. If the outflowsystem is impaired to the point that IOP begins to increase, theeye usually attempts to compensate by reducing the passiveproduction of aqueous humor. Active secretion, however, typicallycontinues at a relatively normal rate, perhaps because if it didnot, the avascular tissues of the eye that rely on aqueous humorfor their nutrition would starve. Because the glaucomatous eye isfunctioning on a greatly diminished percentage of its normallevels of aqueous humor outflow and production, and becauseit has exhausted its usual compensatory pathways, pathologicprocesses or drugs that alter production or outflow only a smallamount can have dramatic effects on IOP. This characteristic isone reason that glaucomatous eyes are typically more responsiveto antiglaucoma drugs than normotensive eyes, but it alsoexplains why IOP can rapidly rise to very high levels in a matterof 1 to 2 hours in some patients.

Often it is difficult to empirically predict the effect a givendrug or its antagonist will have on IOP because many compoundsaffect both aqueous humor production and outflow—sometimesin complex and contradictory ways. For example, stimulationof b-adrenergic receptors in the ciliary processes increasesintracellular cyclic adenosine monophosphate (cAMP), resultingin greater aqueous humor production. b-Adrenergic blockingdrugs (e.g., timolol, betaxolol) decrease cAMP, therebylowering aqueous humor production and ultimately reducingIOP. b-Blockers reduce IOP, however, only if the patient is

awake and adrenergic tone is present. This means that althougha drug such as timolol can reduce IOP in a cat when it is awake,the agent may not control IOP for the more than 20 hours a daythe cat is sleeping.

As expected, b-adrenergic drugs such as epinephrine and itsderivative dipivefrin may transiently increase IOP, presumablyby increasing aqueous humor production via stimulation ofcAMP. A few minutes after application of these drugs, how-ever, IOP begins to decrease, and it stays reduced for severalhours. This is because epinephrine also increases aqueous out-flow via b2 receptors in the trabecular meshwork, and does soto a greater degree than it increases aqueous humor production.Epinephrine may also lower IOP by (1) reducing blood flow tothe ciliary body (thereby lowering aqueous production) and (2) increasing uveoscleral outflow by relaxing the ciliary muscleand recruiting prostaglandins. The latter means, which can beblocked by topical nonsteroidal antiinflammatory drugs, mayresult in further increases in uveoscleral outflow and additionaldecreases in aqueous humor production. Complex interactionssuch as this are but one reason why both b-adrenergic agonistsand b-blockers lower IOP in many species. When one considersspecies and individual differences in the density, distribution,and type of receptors as well as differences in the cause of theglaucoma, it is easy to see why it can be difficult to preciselypredict what effect a given drug will have on IOP in a particularpatient.

Angular aqueous plexus Trabecular meshwork

Scleral venous plexus1

2

3

Figure 12-1. The routes of aqueous drainage from the canine iridocornealangle. Aqueous humor passes between the beamlike pectinate ligament,then through the trabecular meshwork to enter the angular aqueousplexus and eventually the scleral venous plexus. From there, aqueoushumor may drain (1) anteriorly to the episcleral and conjunctival veins,(2) posteriorly into the scleral venous plexus and vortex venous system,or (3) through the ciliary muscle interstitium to the suprachoroid anddiffuse through the sclera (uveoscleral flow). (Modified from Martin CL[1993]: Glaucoma, in Slatter D [editor]: Textbook of Small AnimalSurgery, 2nd ed. Saunders, Philadelphia.)

A

BFigure 12-2. A, The scleral venous plexus is often visible in normalanimals as a series of interwoven blood vessels several millimetersposterior to the limbus. B, Prominent episcleral and, to a lesser extent,conjunctival venous injection in a dog with glaucoma. Increasedintraocular pressure compresses the intrascleral blood vessels, whichdrain posteriorly. This forces more blood through the episcleral andconjunctival veins—one reason the eye appears injected in glaucoma.

SlaOer´s Fundamentals of Veterinary Ophthalmology 4th ed. Saunders, Philadelphia

Causes of Variations in Intraocular Pressure

Diurnal Variation

IOP varies slightly with time of day in many species, being thegreatest in the morning and gradually declining over the courseof the day in dogs and humans. The opposite phenomenon has been suggested to occur in cats, rabbits, and nonhumanprimates.

Age

Both production and outflow of aqueous humor tend to declinewith age, but production declines at a little faster rate than out-flow in most individuals. In humans, aqueous production andIOP tend to decline after 60 years of age, although thistendency varies considerably with ethnic background and thepresence of other diseases, such as systemic hypertension and obesity. Similarly, IOP in cats has been shown to decline approximately 1 mm Hg per year after 7 years of age. In a small percentage of humans, and perhaps animals,however, aqueous humor outflow is reduced to a greater degreethan aqueous humor production, resulting in increased IOPwith age.

Blood Flow

Disorders associated with substantially lower blood flow to the eye (e.g., dehydration, hypovolemic shock, cardio-genic shock) tend to result in lower IOP. A dog collar can significantly increase IOP if the dog is pulling against a leash or if the collar is too tight. Dogs with glaucomaprobably should be exercised with a harness rather than acollar.

Drugs

In addition to the numerous antiglaucoma drugs that alter IOP,other drugs also may affect IOP. Most general anesthetics andtranquilizers cause IOP to fall. Ketamine may temporarilyincrease IOP, presumably owing to extraocular muscle spasm.

Ocular Inflammation

Both spontaneous and surgically induced inflammation loweraqueous production and IOP. A profound reduction in IOP is animportant diagnostic clue to the presence of intraocular inflam-mation, especially uveitis.

DIAGNOSTIC METHODSTonometry

Measurement of and normal values for IOP are discussed inChapter 5. It is suggested that the reader refer to that discussionbefore proceeding with this chapter. Despite its disadvantages, themost economical instrument in general veterinary practice is theSchiøtz tonometer with the human conversion tables. Surprisingly,dog-specific conversion tables for the Schiøtz tonometer do notagree as well with the more accurate applanation and reboundtonometers, and dog specific tables should not be used to convertSchiøtz scale readings to IOP estimates in dogs or cats. Twohandheld tonometers that are more accurate and easier to use thanthe Schiøtz instrument are the Tono-Pen applanation tonometerand the TonoVet rebound tonometer. The ability to performtonometry is essential to every veterinarian engaged in smallanimal practice. Tonometry minimizes the chances of makingan important or even catastrophic error in diagnosis.

IOP should be determined in every red eye with an intactcornea and sclera.

Ophthalmoscopy

Direct and indirect ophthalmoscopy may be used to examinethe optic nerve head for cupping of the optic disc, which is thehallmark of glaucoma. The red-free filter (green light) on manyof these instruments facilitates examination of the optic nerveand retinal nerve fiber layer.

Gonioscopy

Gonioscopy is a very useful technique for examining theiridocorneal (filtration) angle and managing glaucoma. It isdiscussed in detail in Chapter 5. Gonioscopy allows the clini-cian to differentiate between open-angle and closed-angleglaucoma, to estimate the severity of the obstruction of the

232 ! SLATTER’S FUNDAMENTALS OF VETERINARY OPHTHALMOLOGY

Figure 12-3. Common alterations in aqueous production and outflowfacility and their effects on intraocular pressure.

Outflowfacility

Aqueousproduction

Pressure constant Normal state

Outflowconstant

Aqueousproduction falls

Pressure falls Uveitis, drugs

Outflowfalls

Aqueousproduction constant

Pressure rises Glaucoma

SlaOer´s Fundamentals of Veterinary Ophthalmology 4th ed. Saunders, Philadelphia

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Fisiología

•  Drenaje –  Vía convencional (Ángulo iridocorneal)

•  Perro 87% •  Gato 97% •  Caballo 70%

–  Vía alterna\va (Uveoescleral) •  Perro 13% •  Gato 3% •  Caballo 30%

•  Ff •  Ff

–  Dddd –  Fff

•  fff

Fisiología

Angulo iridocorneal normal

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Evaluación del paciente glaucomatoso

•  Tonometría – Gold estándar –  Valor de referencia

•  Perro 16 ± 3 mmHg •  Gato 21 ± 3 mmHg

– Medición = tonometro •  Identación: Schiotz •  Aplanación: Tonopen® •  Rebote: Tonovet®

Tonómetro Tonopen®

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Tonómetro Tonovet®

Tonómetro de Schiotz

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Signos Clínicos

•  BuBalmos •  Ceguera •  Conges\ón bulbar •  Edema corneal •  Estrías de Haab •  Subluxación de cristalino •  Blefaroespasmo

BuBalmos OS

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Conges\ón Bulbar

Luxación Anterior de Cristalino

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Aumento de la PIO

Edema Corneal

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Subluxación de Cristalino

Estrias de Haab

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Diagnós\co

•  Historia •  Signos clínicos •  Tonometría •  Gonioscopía •  Ecograia

GLAUCOMA

1rio 2rio

-‐ Angulo cerrado

-‐ Angulo abierto

-‐ Glaucoma maligno (Sind. de maladirección)

-‐ Tumor IO -‐ Luxación cristalino

-‐ Hifema -‐ Uvei\s -‐ Catarata

intumesecente -‐ Desprendimiento de

re\na -‐ Quistes IO

-‐ Melanosis ocular

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TOP 5 Razas con mayor prevalencia de glaucoma primario -  Cocker Spaniels (5.52%) -  Basset Hound ( 5.44%) -  Chow Chow (4.70%) -  Sharpei (4.70%) -  Boston Terrier (2.88%)

Veterinary Ophthalmology 2014, 7(2): 451

Diagnós\co

•  Historia •  Signos clínicos •  Tonometría •  Gonioscopía •  Ecograia

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1270 Scientific Reports: Retrospective Study JAVMA, Vol 229, No. 8, October 15, 2006

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Glaucoma in dogs is a common, complex, and mul-tifactorial disease in which the flow of aqueous

humor in the eye is impeded by a gross or microscop-ic intraocular abnormality, the IOP increases to valuesincompatible with normal neural function, and theoptic nerve and retina are terminally injured.1-3

Although the terminology for classifying glaucoma in

dogs has been confusing, glaucoma may be broadlycategorized on an etiologic basis as primary or sec-ondary. By use of a number of published definitions,1-9

primary glaucoma may be defined as a breed-related(presumably inherited) condition in which typicallymiddle-aged dogs develop increased IOP in theabsence of other antecedent ophthalmic disease.Affected dogs usually have unilateral disease when firstexamined, but the second eye subsequently becomesaffected. Medical and surgical methods of decreasingIOP remain the mainstay of treatment for all dogs withprimary glaucoma; however, these interventions arenot entirely satisfactory, and treatment is usuallyunsuccessful and results in a nonvisual and painfulglobe. Even with hypotensive treatment, dogs with pri-mary glaucoma are likely to lose vision in the affectedeye within 12 months (median, 8 months) of referral toa veterinary ophthalmologist.1 Prophylactic treatmentincreases the median time to blindness caused by pri-mary glaucoma in the contralateral eye to 31 months,1

but bilateral vision loss is inevitable in most dogs withprimary glaucoma1 despite treatment. Affected dogsshould be removed from breeding programs.

In contrast, secondary glaucoma has beendescribed1-9 as developing in dogs in which high IOP canbe ascribed to 1 or more identifiable primary intraoculardiseases that impede aqueous humor flow within andfrom the eye. Recognized antecedent diseases includeprimary lens dislocation (luxation or subluxation),2,5,9-12

acute or chronic anterior uveitis,2,5,13-15 intraocularcysts,16,17 intumescent cataract formation (phacomorphicglaucoma),18 hyphema,2 intraocular neoplasia,2,19 andocular melanosis (pigmentary glaucoma).20-22 Dogs withsecondary glaucoma may have unilateral or bilateralglaucoma when examined, depending on the primarycause and, although secondary glaucoma is not inherit-ed, the cause of the glaucoma may be. In contrast to pri-mary glaucoma, secondary glaucoma may be successful-ly prevented or treated if the primary disease process isdetected and treated sufficiently early.12 Importantly,even if secondary glaucoma causes loss of vision in 1eye, if the primary condition can be prevented fromoccurring or progressing to cause secondary glaucomain the contralateral eye, total vision loss can be avoided.Therefore, earlier recognition and more aggressive treat-ment of diseases that can lead to secondary glaucoma areessential goals in clinical practice.

Evaluation of risk factors for development of secondary glaucoma in dogs:

156 cases (1999–2004)

Devin A. J. Johnsen, BS; David J. Maggs, BVSc, DACVO; Philip H. Kass, DVM, PhD, DACVPM

Objective—To determine the immediately antecedentcause of secondary glaucoma and the prevalence ofsecondary glaucoma with anterior uveitis or lens dis-location in dogs. Design—Retrospective case series.Animals—156 dogs with secondary glaucoma.Procedures—Cause of glaucoma was determinedfrom records. Breed, age, sex, and neuter status of alldogs with secondary glaucoma were compared withthe general hospital population. The prevalence ofsecondary glaucoma in dogs with a primary diagnosisof lens dislocation or anterior uveitis during the sameperiod was determined. Results—Secondary glaucoma was diagnosed in 156of 2,257 (6.9%) dogs examined because of oph-thalmic disease and was bilateral in 33 (21.2%) ofthose dogs. In 31 (94%) bilaterally affected dogs, theantecedent cause was the same in both eyes.Common causes of secondary glaucoma were non-surgical anterior uveitis (44.9%), anterior uveitis asso-ciated with prior phacoemulsification (15.8%), andlens dislocation (15.2%). Parson Russell Terriers,Poodles, Boston Terriers, Cocker Spaniels, RhodesianRidgebacks, and Australian Cattle Dogs had diag-noses of secondary glaucoma more often thanexpected, compared with the reference population.Age, sex, neuter status, and laterality were not asso-ciated with secondary glaucoma. The prevalence ofsecondary glaucoma in dogs with lens dislocation oruveitis was 15% or 17%, respectively.Conclusions and Clinical Relevance—Glaucomadevelops secondary to many intraocular diseases,particularly uveitis and lens dislocation. Diagnosis ofthese diseases should prompt frequent monitoring ofintraocular pressure, regardless of signalment. (J AmVet Med Assoc 2006;229:1270–1274)

ABBREVIATIONS

IOP Intraocular pressure VMTH Veterinary Medical Teaching Hospital SMR Standardized morbidity ratio

From the Departments of Population Health and Reproduction(Johnsen, Kass) and Surgical and Radiological Sciences (Maggs),School of Veterinary Medicine, University of California, Davis, CA95616.

Supported in part by the UC Davis School of Veterinary MedicineSTAR (Students Training in Advanced Research) Program by a grantfrom the Merck-Merial Veterinary Scholars Research Program.

Address correspondence to Dr. Maggs.

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ABBREVIATIONS





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46.2% and 41.4% spayed females, 36.5% and 35.6%neutered males, 12.2% and 13.6% sexually intact males,and 5.1% and 9.5% sexually intact females; these differ-ences were not significant (P = 0.24). Secondary glauco-ma was diagnosed in 45 breeds and 28 breed crosses.The following breeds were represented by ≥ 5 dogswith secondary glaucoma: Parson Russell Terrier (n =13), Cocker Spaniel (13), Golden Retriever (6),Australian Cattle Dog (5), Labrador Retriever (5), andTerrier cross (5). The number of cases per breed wastoo small to permit significance testing; therefore, SMRwas used to assess the possible effects of breed and wasfound to be high for Parson Russell Terriers (SMR,7.1), Poodles (4.7), Boston Terriers (4.1), CockerSpaniels (3.7), Rhodesian Ridgebacks (4.1), andAustralian Cattle Dogs (3.1). The SMR was decreasedonly in Labrador Retrievers (0.3).

Glaucoma was considered to be secondary to non-surgical anterior uveitis in 71 (44.9%) eyes, anterioruveitis after phacoemulsification in 25 (15.8%) eyes,lens dislocation in 24 (15.2%) eyes, intraocular tumor in17 (10.8%) eyes, anterior uveitis after intracapsular lensextraction in 6 (3.8%) eyes, hyphema in 5 (3.2%) eyes,and cataract in 4 (2.5%) eyes (Figure 2). A markedly

narrowed anterior chamber with presumed pupillaryblock was recorded for all 4 eyes (3 dogs) in whichcataracts were considered to be the primary cause ofglaucoma. Although all 4 of those eyes had signs of pre-vious anterior uveitis, signs of active uveitis (aqueousflare) were noted in only 1 of those 4 eyes at the timeglaucoma was diagnosed. The immediately antecedentcause of glaucoma could not be adequately determinedin 6 (3.8%) eyes with secondary glaucoma. No signifi-cant effects of sex and neuter status, age, or laterality onthe cause of secondary glaucoma were detected.

The right eye only was affected in 60 (38.5%) dogs,the left eye only was affected in 63 (40.4%) dogs, andboth eyes were affected in 33 (21.2%) dogs. No signifi-cant difference in sex and neuter status or age wasdetected between dogs with unilateral secondary glau-coma and those with bilateral disease. No differenceswere detected between the 2 groups in breeds affected.However, the overall distribution of causes was differentbetween dogs with unilateral or bilateral secondary glau-coma (P = 0.049). This difference was a result of theabsence of intraocular tumor or hyphema as a primarydiagnosis in any dog with bilateral secondary glaucoma.In 31 of the 33 (94%) dogs with bilateral secondaryglaucoma, the same antecedent cause was detected inboth eyes. In the remaining 2 dogs, glaucoma was con-sidered to be secondary to lens dislocation in 1 eye andsecondary to anterior uveitis associated with intracapsu-lar lens extraction for lens dislocation in the other. In thesecond part of the study, the prevalences of secondaryglaucoma in dogs with a primary diagnosis of lens dis-location or uveitis were 15% and 17%, respectively, dur-ing the 5-year period reviewed. However, accurateassessment of how rapidly secondary glaucoma devel-oped in individual dogs was not possible.

DiscussionIn the present study, secondary glaucoma was

diagnosed in approximately 7% of all dogs examinedfor ophthalmic disease at this referral institution.These data are similar to those from another report9 inwhich glaucoma represented 8.6% of ophthalmic diag-noses. In the study reported here, secondary glaucoma

was diagnosed most frequently in eithereye of middle-aged to older dogs ofeither sex and irrespective of neuter sta-tus. Overrepresented breeds includedthe Parson Russell Terrier, Poodle,Boston Terrier, Cocker Spaniel,Rhodesian Ridgeback, and AustralianCattle Dog; however, many breeds andage groups were represented. Of the fre-quently affected breeds, the BostonTerrier, Cocker Spaniel, and Poodle haveall been reported by other authors3,25 asbeing affected by primary glaucoma, andthis finding has been supported by his-tologic or gonioscopic confirmation ofgoniodysgenesis in Cocker Spaniels.13,26

This finding highlights a problem inher-ent in the assumption that primary andsecondary glaucoma are mutually exclu-sive. Rather, it seems reasonable that an

Figure 2—Relative frequency of ocular diseases diagnosed and considered to resultin secondary glaucoma in 158 eyes from the same 156 dogs in Figure 1. Shaded por-tions represent all dogs with uveitis.

Figure 1—Distribution by age of dogs with secondary glaucomaand those in an unaffected reference population in a retrospec-tive study of 156 dogs examined at a referral institution becauseof ophthalmic disease.

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49.7%

15.8%

15.2%

10.8%


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156 cases (1999–2004)



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156 cases (1999–2004)



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ì  Servicio de oBalmología Universidad de California Davis ì  1 Julio 1999 a 30 Junio 2004 (5 años) ì  2257 perros ì  156 (6.9%) casos glaucoma 2rio ì  Parson Russell Terrier ì  Cocker Spaniel ì  Golden Retriever ì  Pastor Australiano

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Glaucoma Secundario a Uvei\s Anterior OS

Tratamiento

•  Médico – Análogos prostaglandinas •  P ej: Latanoprost

–  Inhibidores de anhidrasa carbónica tópicos •  P ej: Dorzolamida

–  Inhibidores anhidrasa carbónica sistémicos •  P ej: Acetazolamida

Compendium 2009, 31(10): 454-‐58

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Tratamiento

•  Médico – Hiperosmó\cos •  P ej: Manitol

– Otros medicamentos •  β-‐bloqueadores

–  P ej: Timolol

•  Colinérgicos –  P ej: Pilocarpina

Compendium 2009, 31(10): 454-‐58

Tratamiento

•  Médico – Neuroprotección •  Obje%vo: Proteger y prolongar la sobrevida de las células ganglionares intactas y sanas •  Áreas de trabajo:

–  Efecto mecánico –  Efecto isquémico –  Efecto reperfusión

Consulta de Difusión Veterinaria 2010, 17: 454-‐58

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Tratamiento

•  Médico – Neuroprotección •  Efecto mecánico

–  > PIO –  Lamina cribosa –  Alteración flujo axoplásmico

»  < Neurotrofinas »  Factor neurotrófico derivado del cerebro


Tratamiento

•  Médico – Neuroprotección

•  Efecto isquémico –  > glutamato = exitotoxicidad

»  Receptor N-‐me\l D-‐aspartato (NMDA) »  Neurotransmisor a > toxico »  > Calcio intracelular


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Tratamiento


•  Efecto isquémico –  > glutamato = exitotoxicidad

»  > Oxido nitroso = vasodilatación »  > Endotelina-‐1 »  > Radicales libres

–  Apoptosis


Tratamiento


•  Neman%na –  Actúa sobre efecto isquémico –  Bloqueador receptor NMDA –  Previene efectos tóxicos del glutamato

Centro Veterinario 2013, 55: 4-‐21

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Tratamiento


•  Amlodipino –  Efecto isquémico –  Bloqueador canales de calcio –  Disminuye la entrada de calcio –  < Oxido nitroso

Centro Veterinario 2013, 55: 4-‐21

Tratamiento


•  Melatonina –  An\oxidante –  Administración oral <PIO humanos y monos –  > factores neurotróficos –  Promueve sobrevivencia de cel. ganglionares –  Incrementa tasa de sobrevivencia, rescate y restauración de cel. ganglionares en casos x isquemia reperfusión

Ophthalmic Physiol Opt 20135 35(2): 201-‐5

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Tratamiento


•  Melatonina –  Hormona sinte\zada a par\r de la serotonina –  Par\cipa en regulación del ciclo circadiano –  Producción cuerpo ciliar y re\na –  Receptores M1 y M2 = Re\na, coroides y vasculatura re\nal –  Regulación PIO x medio del ciclo circadiano –  Triptophan® = aminoácido esencial precursor de la serotonina

Chonnam Med J 2013 48(2): 116-‐22

Tratamiento


•  Extracto de semilla de uva –  Proantocianidina

»  An\oxidante > vit C y E »  Barredor radicales libres »  An\inflamatorio

Food Chem Toxicol 2009, 47: 198-‐204

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Tratamiento


•  Ácidos grasos –  > respuesta bastones –  Protección re\na y vascularización

»  Inflamación »  Isquemia »  Luz

–  Pelo & Derme® = Suplemento con alto contenido de ácidos grasos esenciales omega 3 y 6.

Prog Re\n Eye Res 2005, 47: 87-‐138

Tratamiento


•  Zinc –  An\oxidante –  Compite con el hierro reduciendo el ciclo redox –  Unida a la Vit E reduce la peroxidación lipidica –  Importante en la salud de la re\na y funcion de la Vit A –  Pelo & Derme® = Suplemento alimen\cio que con\ene Zinc

Free Radic Biol Med 2001, 31: 266-‐74

Free Radic Biol Med. 2001; 31: 266-‐274.

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Tratamiento


•  Vit E –  An\oxidante lipofilico –  La Vit E es oxidiadizada a tocoferaxol el cual ayuda a mantener los niveles de tocoferol

– Mayor an\oxidante presente en las células –  En humanos efecto protector en degeneración macular relacionada con la edad

–  Pelo & Derme® = Suplemento alimen\cio que con\ene Vit E

Ophthal Physiol Opt 2004, 24: 339-‐49

Ophthal Physiol Opt. 2004; 24: 339-‐349.

VILLA DE LEYVA (COLOMBIA)

plantilla programa ciencia. glaucomoa

Health & Medicine