ABSTRACT
Twenty normal Golden Retrievers being screeened for eye, hip and elbow diseases were given tropicamide topically and medetomidine systemically. Medetomidine effects were later reversed with systemic atipamezole. Pupil size and intraocular pressure changes were determined. Pupil size increased significantly following tropicamide administration and continued to increase slightly but significantly after medetomidine injection. It was unclear whether the slight increase in pupil size following medetomidine administration was due to continued effect of tropicamide or due to the medetomidine itself. Atipamezole did not influence pupil size. Intraocular pressure (IOP) was not affected by these drugs. Ophthalmic screening examination for inherited disease following tropicamide administration is equally feasible prior to sedation with medetomidine and after reversal with atipamezole, but not during the period of sedation.
Subject(s)
Dogs/physiology , Imidazoles/pharmacology , Intraocular Pressure/drug effects , Medetomidine/pharmacology , Mydriatics/pharmacology , Pupil/drug effects , Tropicamide/pharmacology , Administration, Oral , Administration, Topical , Adrenergic alpha-Antagonists/administration & dosage , Adrenergic alpha-Antagonists/pharmacology , Animals , Female , Hypnotics and Sedatives/administration & dosage , Hypnotics and Sedatives/pharmacology , Imidazoles/administration & dosage , Male , Medetomidine/administration & dosage , Mydriatics/administration & dosage , Reference Values , Tropicamide/administration & dosageABSTRACT
Between 1989 and 1997, 8204 rough collies were examined for collie eye anomaly (CEA) at up to 10 weeks of age. All dogs were positively identified and the results were registered under the Swedish Kennel Club genetic health programme. A significant decrease in litter size occurred if one of two affected parents had coloboma (3.8 pups) compared with litters from two chorioretinal dysplasia- (CRD-) affected collies (5.2 pups) or litters by two normal collies (5.0 pups), indicating an influence of the coloboma genotype on offspring vitality. The prevalence of CRD in pups from normal x normal matings and CRD x CRD matings was significantly different from that expected under simple autosomal recessive inheritance (43 per cent versus 25 per cent and 85 per cent versus 100 per cent). The results are compatible with polygenic inheritance but not with simple autosomal recessive inheritance. CRD prevalence in offspring of CRD x coloboma matings was significantly lower than in pups of CRD x CRD matings, reflecting effects of the coloboma genotype on vitality. These results have important implications for breeding programmes and the genetic control of CEA.
Subject(s)
Animal Husbandry , Dog Diseases/genetics , Eye Abnormalities/veterinary , Animals , Breeding , Chorioretinitis/epidemiology , Chorioretinitis/genetics , Chorioretinitis/veterinary , Coloboma/epidemiology , Coloboma/genetics , Coloboma/veterinary , Dog Diseases/epidemiology , Dog Diseases/prevention & control , Dogs , Eye Abnormalities/epidemiology , Eye Abnormalities/genetics , Female , Litter Size , Male , Prevalence , Retinal Dysplasia/epidemiology , Retinal Dysplasia/genetics , Retinal Dysplasia/veterinary , Sweden/epidemiologyABSTRACT
A total of 8204 rough collies, representing 76 per cent of all collies registered by the Swedish Kennel Club between 1989 and 1997, were examined before 10 weeks of age for collie eye anomaly (CEA). All dogs were permanently identified and examination results were registered and computerised. The policy of breeders during the study period was to select against coloboma in breeding stock, but to allow breeding of chorioretinal dysplasia (CRD) affected animals. The prevalence of CRD increased significantly from 54.2 per cent to 68.1 per cent (P < 0.001) from 1989 to 1997, while the prevalence of coloboma did not (8.3 per cent to 8.5 per cent, P = 0.4). These results are not compatible with a simple, recessive, autosomal inheritance for the entire CEA complex.
