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Vitreous and retinal amino acid concentrations in experimental central retinal artery occlusion in the primate
Journal article   Open access   Peer reviewed

Vitreous and retinal amino acid concentrations in experimental central retinal artery occlusion in the primate

Y H Kwon, D W Rickman, S Baruah, M B Zimmerman, C-S Kim, H C Boldt, S R Russell and S S Hayreh
Eye (London), Vol.19(4), pp.455-463
04/2005
DOI: 10.1038/sj.eye.6701546
PMID: 15184939
url
https://doi.org/10.1038/sj.eye.6701546View
Published (Version of record) Open Access

Abstract

Vitreous and retinal amino-acid concentrations were evaluated in a primate model of central retinal artery occlusion (CRAO) to study the role of glutamate excitotoxicity in acute retinal ischaemia. Unilateral, acute CRAO was produced by temporary clamping of the central retinal artery for 190 min in four elderly rhesus monkeys. Fundus photography, fluorescein angiography, and electroretinogram were performed before and during CRAO, and after unclamping the artery. Vitreous samples were obtained before and after CRAO in both eyes, and analysed for 13 amino-acid concentrations using high-pressure liquid chromatography. The animals were killed 350 min after retinal reperfusion, and the retinal tissue was submitted for amino-acid analysis. In all four eyes, the macula showed the 'cherry red spot'. The CRAO was confirmed by fluorescein angiography and decreased b-wave on electroretinogram. Retinal histology confirmed ischaemic changes in the inner retina. Changes in all 13 vitreous amino-acid concentrations after CRAO (including glutamate) were not significantly different between study and control eyes (P = 0.09 to 0.82). All retinal amino-acid concentrations (including glutamate) were not significantly different between two eyes (P = 0.07-0.93). In the primate model of acute inner retinal ischaemia induced by transient CRAO, we were unable to detect significantly elevated concentrations of vitreous and retinal glutamate. Our primate model has the advantage of closely modelling the CRAO in humans. Further basic and clinical studies are needed to elucidate the role of glutamate excitotoxicity in retinal ischaemia.
Electroretinography Acute Disease Retina - metabolism Chromatography, High Pressure Liquid - methods Fluorescein Angiography - methods Specimen Handling - methods Macaca mulatta Amino Acids - metabolism Retinal Artery Occlusion - metabolism Animals Vitreous Body - metabolism Glutamic Acid - metabolism Retinal Artery Occlusion - etiology Fundus Oculi Disease Models, Animal

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