O maleato de timolol 0,5% é um fármaco recomendado para tratamento de glaucoma em cães. Após instilação, e absorvido para a circulação sistêmica e por ser um antagonista beta-adrenérgico pode promover efeitos colaterais sistêmicos importantes sobre a condução elétrica cardíaca. No presente estudo, foi avaliada a alteração causada pelo timolol 0,5% oftálmico no eletrocardiograma. Foram selecionados seis cães hígidos para participar de dois tratamentos oftálmicos diferentes: no primeiro foi instilado placebo (hipromelose 0,5%) e no segundo utilizou-se timolol 0,5%. O colírio foi instilado a cada 12 horas por 14 dias. Os parâmetros eletrocardiográficos foram mensurados nos tempos: zero, 10, 60, 120, 240, 360 e 720 minutos após instilação da solução ocular nos dias primeiro, sétimo e décimo quarto de cada tratamento. As alterações eletrocardiográficas foram mais evidentes entre 120 e 240 minutos pós-instilação de timolol 0,5% quando comparado com o tratamento placebo. O ritmo foi irregular, com momentos de arritmia sinusal e bradicardia sinusal. Os intervalos RR e PR prolongaram significativamente (p < 0,05) desde o primeiro dia de instilação de timolol, sendo o prolongamento mais expressivo no décimo quarto dia de tratamento. O intervalo QT demonstrou pouca variação, apenas prolongando significativamente (p < 0,05) no décimo quarto dia de aplicação de timolol. O intervalo QTc não demonstrou alteração significativa (p > 0,05). Apesar das alterações encontradas, não foram observadas manifestações clínicas relacionadas ao timolol nos animais estudados. Deve-se considerar, porém, que os animais em questão eram hígidos e, portanto, as alterações decorrentes do uso do timolol em animais com cardiopatias preexistentes poderiam promover sinais clínicos, sendo recomendada a avaliação cardíaca de pacientes previamente à prescrição do timolol oftálmico.

OBJECTIVE: To assess changes in pupil size and intraocular pressure (IOP) following topical application of a 0.5% tropicamide solution in the eyes of healthy butorphanol-sedated dogs. ANIMALS: 12 healthy adult Beagles. PROCEDURES: In a randomized crossover study consisting of 2 treatment periods with a 1-week washout between periods, dogs received an IM injection of butorphanol (0.2 mg/kg) or an equal volume of sterile saline (0.9% NaCl) solution. For each dog, 1 drop of 0.5% tropicamide ophthalmic solution was topically instilled in one eye and 1 drop of artificial tear solution was topically instilled in the other eye 10 minutes after the IM injection and again 5 minutes later. Extent of sedation, pupil size, and IOP were evaluated from 20 minutes before to 80 minutes after the IM injection and compared among treatment combinations. RESULTS: Butorphanol induced mild (n = 9) or moderate (3) sedation in all dogs and slightly delayed the onset of, but did not prevent, tropicamide-induced mydriasis. Butorphanol caused a significant increase in IOP, which was not exacerbated by tropicamide-induced mydriasis; however, that increase was generally not sufficient to exceed the upper limit of the IOP reference range. CONCLUSIONS AND CLINICAL RELEVANCE: Results indicated that butorphanol did not prevent tropicamide-induced mydriasis but did increase the IOP in ophthalmologically normal Beagles. Although the butorphanol-induced increase in IOP did not appear clinically relevant for the dogs of this study, that may not be true for dogs with glaucoma, and care should be taken when butorphanol is administered to such dogs.

OBJECTIVE To determine the intraocular pressure (IOP) in healthy dromedary camels (Camelus dromedarius). ANIMALS 24 clinically normal dromedary camels. PROCEDURES For each camel, the IOP of both eyes was measured with applanation tonometry. Three measurements with < 5% variance were obtained for each eye on the same day of the week for 3 consecutive weeks. Mean IOP was calculated for each eye on each day for comparison purposes. RESULTS Mean ± SD IOPs for the right (31.1 ± 2.1 mm Hg) and left (30.8 ± 1.9 mm Hg) eyes of immature camels were significantly higher than those for the right (27.1 ± 1.2 mm Hg) and left (28.2 ± 1.2 mm Hg) eyes of mature camels. Intra-assay and interassay coefficients of variation (CVs) for IOP measurements of the right and left eyes did not differ significantly between immature and mature camels. Interassay CVs of IOP measurements for the right and left eyes ranged from 1.5% to 12.1% and 1.2% to 10.3%, respectively, for immature camels and from 1.2% to 17.2% and 1.7% to 18.8%, respectively, for mature camels. Intra-assay CVs of IOP measurements for the right and left eyes ranged from 1.5% to 10.6% and 1.9% to 9.6%, respectively, for immature camels and from 2.8% to 16.9% and 2.7% to 12.4%, respectively, for mature camels. Age was negatively correlated (r = −0.403) with IOP. CONCLUSIONS AND CLINICAL RELEVANCE Results provided a reference and might aid in the diagnosis of glaucoma and uveitis during complete ophthalmic examinations of dromedary camels.

The effects of mitomycin-C on intraocular pressure (IOP), facility of outflow (C), and Tenon's capsule fibrosis were studied over 60 days in 10 clinically normal dogs. A 1-piece, silicone glaucoma implant was surgically implanted into both eyes; the filtration site of one eye was treated with a single, 5-minute intraoperative application of mitomycin (0.5 mg/ml), and the fellow eye was treated in a similar manner with balanced salt solution. There were no significant differences in preoperative IOP or C-values between treatment groups. Mean IOP in eyes of both groups initially decreased from the preoperative value, but returned to the baseline value by day 21. Mean facility of aqueous outflow (C-value) increased in all eyes during the first 14 days (mitomycin-C-value = 2.26 +/- 0.72; control C-value = 2.38 +/- 0.81), then reached a plateau that was significantly higher than the baseline value in mitomycin (P = 0.039) and control (P = 0.041) eyes. Histologic evaluation revealed all implants surrounded by a connective tissue capsule composed of regular dense collagen and fibroblasts that was significantly (P = 0.003) thinner in the mitomycin-treated (scleral side = 167 +/- 62 micrometer; conjunctival side = 122 +/- 41 micrometer) than the control (scleral side = 261 +/- 92 micrometer; conjunctival side = 180 +/- 48 micrometer) group. There were, however, no significant differences in IOP or C-values between groups at any postoperative time interval. Results of this study indicate that intraoperative treatment with mitomycin suppresses, but does not prevent fibrosis around silicone filtering implants.

Ocular biometry, using A-scan ultrasonography and ultrasonographic pachymetry, was performed in 52 Samoyeds, 2 months to 13 years old, without intraocular or systemic diseases. Furthermore, the relative depth of the opening of the ciliary cleft was estimated from goniophotographs. The values were analyzed, and statistical models of changes in ocular distances with increasing age were identified. It was found that the changes in corneal thickness, axial anterior chamber depth, lens thickness, relative lens position, length of the vitreous body, and axial length could best be described by 1 of the 2 nonlinear models (...). The course began with a period of rapid increase, after which the ocular distance either increased at a progressively slower rate toward infinity (corneal and lens thickness) or to a finite limit (relative lens position and axial length), or ceased to grow and finally started to decrease toward minus infinity (axial anterior chamber depth and length of the vitreous body). However, suitable model for determining relative depth of the opening of the ciliary cleft could not be established. Results indicated that age-related changes, mainly in lens thickness, cause a shallow anterior chamber, and it was suggested that this may be of importance for development of a relative pupillary block and, thus, primary angle-closure glaucoma, at least in preconditioned eyes of Samoyeds.

The anterior chambers in 16 dogs with normotensive eyes and 3 Beagles with glaucomatous eyes were treated with 0, 25, 50, or 100 IU of bovine testicular hyaluronidase. Aqueous outflow resistance was then determined by constant-pressure perfusion of 0.9% NaCl solution for 30 or 60 minutes. In normotensive eyes, 25, 50, or 100 IU of hyaluronidase significantly (P < 0.02) increased the rate of constant-pressure perfusion compared with that of untreated eyes during 30- or 60-minute perfusions. Treatment of glaucomatous eyes with 25, 50, or 100 IU of hyaluronidase did not significantly increase the rate of constant-pressure perfusion over controls during a 30-minute perfusion. Bovine testicular hyaluronidase at all doses removed the staining of colloidal iron from the trabecular meshwork in normotensive eyes. In Beagles with glaucoma, the trabecular meshworks remained stained with colloidal iron when treated with the hyaluronidase, which suggested that some glycosaminoglycans were resistant to this enzyme's action.

Numbers of mast cells in the cornea, sclera, choroid, ciliary body, iris, and retina of sections of globes from 35 clinically normal dogs and 34 dogs with secondary glaucoma was determined. Fixed globes were trimmed along a vertical midsagittal plane and embedded in paraffin. Tissue sections, approximately 6 micrometer thick, were stained with toluidine blue for identification of mast cells. In normal globes, most of the mast cells were observed in the anterior portion of the uvea, and fewer mast cells were seen in the choroid and sclera. Mast cells were not observed in the retina and were seldom observed in the cornea of dogs with or without glaucoma. In sections of glaucomatous globes, mast cells were distributed evenly in the uvea and sclera, and fewer mast cells were present than in normal globes, regardless of the cause of glaucoma.

OBJECTIVE To evaluate the coding regions of ADAMTS17 for potential mutations in Chinese Shar-Pei with a diagnosis of primary open-angle glaucoma (POAG), primary lens luxation (PLL), or both. ANIMALS 63 Shar-Pei and 96 dogs of other breeds. PROCEDURES ADAMTS17 exon resequencing was performed on buccal mucosal DNA from 10 Shar-Pei with a diagnosis of POAG, PLL, or both (affected dogs). A candidate causal variant sequence was identified, and additional dogs (53 Shar-Pei [11 affected and 42 unaffected] and 95 dogs of other breeds) were genotyped for the variant sequence by amplified fragment length polymorphism analysis. Total RNA was extracted from ocular tissues of 1 affected Shar-Pei and 1 ophthalmologically normal Golden Retriever; ADAMTS17 cDNA was reverse transcribed and sequenced, and ADAMTS17 expression was evaluated by quantitative reverse-transcription PCR assay. RESULTS All affected Shar-Pei were homozygous for a 6-bp deletion in exon 22 of ADAMTS17 predicted to affect the resultant protein. All unaffected Shar-Pei were heterozygous or homozygous for the wild-type allele. The variant sequence was significantly associated with affected status (diagnosis of POAG, PLL, or both). All dogs of other breeds were homozygous for the wild-type allele. The cDNA sequencing confirmed presence of the expected variant mRNA sequence in ocular tissue from the affected dog only. Gene expression analysis revealed a 4.24-fold decrease in the expression of ADAMTS17 in ocular tissue from the affected dog. CONCLUSIONS AND CLINICAL RELEVANCE Results supported that the phenotype (diagnosis of POAG, PLL, or both) is an autosomal recessive trait in Shar-Pei significantly associated with the identified mutation in ADAMTS17.

Objective: To determine the effects of topically applied 2% delta-9-tetrahydrocannabinol (THC) ophthalmic solution on aqueous humor flow rate (AHFR) and intraocular pressure (IOP) in clinically normal dogs. Animals: 21 clinically normal dogs. Procedures: A randomized longitudinal crossover design was used. Following acquisition of baseline IOP (morning and evening) and AHFR (afternoon only) data, dogs were randomly assigned to 2 treatment groups and received 1 drop of either 2% THC solution or a control treatment (olive oil vehicle) to 1 randomly selected eye every 12 hours for 9 doses. The IOPs and AHFRs were reassessed after the final treatment. Following a washout period of ≥ 7 days, dogs were administered the alternate treatment in the same eye, and measurements were repeated. Results: Mean ± SD IOPs in the morning were 15.86 ± 2.48 mm Hg at baseline, 12.54 ± 3.18 mm Hg after THC treatment, and 13.88 ± 3.28 mm Hg after control treatment. Mean ± SD IOPs in the evening were 13.69 ± 3.36 mm Hg at baseline, 11.69 ± 3.94 mm Hg after THC treatment, and 12.13 ± 2.99 mm Hg after control treatment. Mean IOPs were significantly decreased from baseline after administration of THC solution but not the control treatment. Changes in IOP varied substantially among individual dogs. Mean ± SD AHFRs were not significantly different from baseline for either treatment. Conclusions and Clinical Relevance: Topical application of 2% THC ophthalmic solution resulted in moderate reduction of mean IOP in clinically normal dogs. Further research is needed to determine efficacy in dogs with glaucoma.

Objective-To investigate whether differences existed between clinically normal dogs and dogs with goniodysgenesis-related glaucoma (GDRG) in serum autoantibodies against optic nerve antigens. Animals-16 dogs with GDRG, 17 healthy dogs with unremarkable pectinate ligament and iridocorneal angle morphology, and 13 euthanized dogs with no major ocular abnormalities or underlying diseases. Procedures-Western blotting was performed with optic nerve extracts from the euthanized dogs as an antigen source and serum from clinically normal dogs and dogs with GDRG as a primary antibody (autoantibody) source. Blots were evaluated for presence and density of bands. Results-Multiple bands were identified on western blots from all dogs with GDRG and all clinically normal dogs, with a high degree of variability among individual dogs. Dogs with GDRG were significantly more likely than healthy dogs to have bands present at 38, 40, and 68 kDa. Dogs with GDRG had significant increases in autoreactivity at 40 and 53 kDa and a significant decrease in autoreactivity at 48 kDa. Conclusions and Clinical Relevance-Significant differences in serum autoantibodies against optic nerve antigens were found in dogs with versus without GDRG. Although it remains unclear whether these differences were part of the pathogenesis of disease or were sequelae to glaucomatous changes, these findings provide support for the hypothesis that immune-mediated mechanisms play a role in the development or progression of GDRG. However, the high degree of variability among individual dogs and the considerable overlap between groups suggest that the clinical usefulness of this technique for distinguishing dogs with GDRG from clinically normal dogs is likely limited.