DECREASED NO RELEASE IS A WORSENING FACTO R IN BRANCH VEIN OCCLUSION

Purpose Following retinal branch vein occlusion (b.v.o.), the arteriol e crossing the occluded territories' is often constricted. This constr iction persists up to several weeks and is correlated with the develop ment of extended territories of non-perfused capillaries. We present h ere results of an investigation supporting the hypothesis that decreas e in the production of nitric oxide (NO) accounts for the observed art eriolar constriction. Methods Preretinal [NO] was measured using an NO microprobe in the anesthethized miniature pigs, before and within the first 4 hours following experimental b.v.o.. Modifications of arterio lar diameter were correlated to preretinal [NO] changes. The retinal a rteriolar sensitivity to constitutive NO was checked by performing pre retinal puff injections of nitro-1-arginine (L-NA) after both systemic hypoxia and b.v.o. Results Two hours after b.v.o, there was 73.7 +/- 4% decrease in preretinal [NO] and a simultaneous 25.4 +/- 3.4 % decre ase in the diameter of the arteriole in the affected territory. Both p ersisted for at least 4 hours after b.v.o.. Puffing L-NA over an arter iole previously dilated by systemic hypoxia induced a vasoconstriction . However no arteriolar constriction was observed when puffing was per formed on an arteriole after b.v.o. Conclusions These results show tha t experimental b.v.o. induces in the affected retina an impairment in the release of constitutive NO and an arteriolar constriction, which i n turn, contribute to the development of tissue hypoxia and neuronal s welling and death in the inner retina.