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[Endogenous deficiency of nitric oxide as an aggravating factor in retinal vein occlusion].

PURPOSE
Following retinal branch vein occlusion (b.v.o.), the arteriole crossing the occluded territories is often constricted. This constriction persists up to several weeks and is correlated with the development of extended territories of non-perfused capillaries. We present here results of an investigation supporting the hypothesis that decrease in the production of nitric oxide (NO) accounts for the observed arteriolar 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 arteriolar diameter were correlated to preretinal [NO] changes. The retinal arteriolar sensitivity to constitutive NO was checked by performing preretinal 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% decrease in the diameter of the arteriole in the affected territory. Both persisted for at least 4 hours after b.v.o. Puffing L-NA over an arteriole previously dilated by systemic hypoxia induced a vasoconstriction. However no arteriolar constriction was observed when puffing was performed on an arteriole after b.v.o.


CONCLUSIONS
These results show that experimental b.v.o. induced in the affected retina an impairment in the release of constitutive NO and an arteriolar constriction, which in turn, contribute to the development of tissue hypoxia and neuronal swelling and death in the inner retina.