According to literature reports, primary glaucoma, also known as hereditary glaucoma, has been found in animals such as rabbits, dogs, cats, monkeys, and mice. Gelatt believes that an ideal animal model for primary glaucoma can be passaged through a simple genetic pattern; Display obvious onset and clinical process of glaucoma; There is a sufficiently long period before glaucoma causes eye damage for anatomical, physiological, pathological, and pharmacological research. At present, the application research of rabbits is the most extensive, followed by dogs. Primary glaucoma in rabbits is characterized by autosomal recessive inheritance during the semi reactive phase, which can occur in both white and colored rabbits. Knepper et al. believe that primary glaucoma in rabbits is an autosomal recessive gene with incomplete exoneration. Rabbits with homozygous conjugates of the primary glaucoma gene exhibit elevated intraocular pressure and develop glaucoma at 5-6 months of age after birth. This type of primary glaucoma in rabbits is believed to be caused by undifferentiated uveal tissue in the anterior chamber.
Further research by Knepper et al. suggests that the most likely cause of angle morphology defects in primary glaucoma in rabbits is the loss of function of differentiation genes controlling the endothelial cells of the trabecular meshwork within and between the trabecular spaces, both at the entrance of the trabecular meshwork and within the trabecular meshwork layer. Due to its resemblance to congenital glaucoma in the human eye, the author believes that rabbits can serve as animal experimental models for understanding and treating congenital glaucoma in the human eye.
Glaucoma in non primate species is most common in dogs. Glaucoma in dogs is often primary and manifests as familial or hereditary. Samuelson et al. believe that primary glaucoma in dogs has the characteristic of autosomal recessive inheritance, where intraocular pressure begins to increase at 9-12 months of age and becomes a chronic process of binocularity. Gelatt et al. classified the clinical manifestations of hereditary glaucoma in 55 hunting dogs into three stages: early, moderate, and late. In the early stage, the appearance of the anterior chamber angle was normal, the intraocular pressure was 30-35mmHg, and the optic nerve and optic disc were normal; In the middle stage, there is a narrow angle or even a slight closure of the angle, and some of the suspensory ligaments of the lens lose attachment, resulting in lens subluxation and optic disc depression; The late stage angle presents as a narrow angle to a closed angle, with high intraocular pressure, corneal edema, dilated optic disc depression, and optic nerve atrophy. The early and mid-term course of primary glaucoma in dogs before angle closure and lens dislocation can be used as an experimental animal model for studying primary open-angle glaucoma. Peiffer and Gelatt believe that changes in atrial angle are secondary to changes in lens dislocation, supporting the hypothesis that primary glaucoma in dogs is open angle glaucoma. Histopathological studies have shown that the trabecular meshwork structure disorder characterized by the accumulation of extracellular substances in the outflow channel of aqueous humor is a characteristic of this condition. No association was found between narrow angle of the room and elevated intraocular pressure. They believe that the early manifestation of primary glaucoma in dogs is most similar to human primary open angle glaucoma in animal spontaneous glaucoma.