J C Lai1, M W Johnson, C L Martonyi, G O Till. 1. W.K. Kellogg Eye Center, Department of Ophthalmology, University of Michigan School of Medicine, Ann Arbor, USA.
Abstract
PURPOSE: To develop an animal model of complement-induced retinal vasculopathy and determine whether it resembles Purtscher's retinopathy. METHODS: Intravenous cobra venom factor was used to achieve intravascular activation of the complement system in cats. After a single bolus of cobra venom factor (75 units/kg), retinal blood flow was monitored at regular intervals by fluorescein angioscopy and angiography. RESULTS: Multiple small retinal arteriolar occlusions were present during the initial fluorescein transit of the immediate postinjection fluorescein study in 12 of 12 animals. Small, rapidly moving gaps in the fluorescein column were seen in two thirds of the animals observed continuously by fluorescein angioscopy. Angiographically, the obstructions were transient, and filling of the associated patches of capillary nonperfusion occurred within 3 minutes. Purtscher's-like ischemic retinal infarcts did not develop in any eye. Histopathologic analysis failed to demonstrate the nature of the transient vascular obstructive lesions, but indirect evidence suggested the possibility of granulocyte aggregates. CONCLUSION: Intravascular activation of the complement system produces transient microembolic retinal arteriolar occlusions in the cat. Although this model may represent a mild form of Purtscher's retinopathy, factors in addition to complement activation appear necessary to induce ischemic retinal infarcts.
PURPOSE: To develop an animal model of complement-induced retinal vasculopathy and determine whether it resembles Purtscher's retinopathy. METHODS: Intravenous cobra venom factor was used to achieve intravascular activation of the complement system in cats. After a single bolus of cobra venom factor (75 units/kg), retinal blood flow was monitored at regular intervals by fluorescein angioscopy and angiography. RESULTS: Multiple small retinal arteriolar occlusions were present during the initial fluorescein transit of the immediate postinjection fluorescein study in 12 of 12 animals. Small, rapidly moving gaps in the fluorescein column were seen in two thirds of the animals observed continuously by fluorescein angioscopy. Angiographically, the obstructions were transient, and filling of the associated patches of capillary nonperfusion occurred within 3 minutes. Purtscher's-like ischemic retinal infarcts did not develop in any eye. Histopathologic analysis failed to demonstrate the nature of the transient vascular obstructive lesions, but indirect evidence suggested the possibility of granulocyte aggregates. CONCLUSION: Intravascular activation of the complement system produces transient microembolic retinal arteriolar occlusions in the cat. Although this model may represent a mild form of Purtscher's retinopathy, factors in addition to complement activation appear necessary to induce ischemic retinal infarcts.
Authors: J E Ramos de Carvalho; R O Schlingemann; M Oranje; F J Bemelman; M J van Schooneveld Journal: Int Ophthalmol Date: 2017-03-08 Impact factor: 2.031