Donati G, Pournaras C J, Pizzolato G P, Tsacopoulos M
Department of Clinical Neuroscience, University of Geneva Medical School, Switzerland.
Invest Ophthalmol Vis Sci. 1997 Jun;38(7):1450-7.
After retinal branch vein occlusion (BVO), 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 nonperfused capillaries. These are results of an investigation supporting the hypothesis that decrease in the production of nitric oxide (NO) accounts for the observed arteriolar constriction.
Preretinal [NO] was measured using an NO microprobe in the anesthetized miniature pigs, before and during the first 4 hours after experimental branch vein occlusion. Modifications of arteriolar diameter were correlated to preretinal [NO] changes. The retinal arteriolar sensitivity to constitutive NO was checked by applying preretinal puff injections of nitro-L-arginine (L-NA) after both systemic hypoxia and branch vein occlusion.
Two hours after branch vein occlusion there was a 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 branch vein occlusion. Applying a puff of L-NA to an arteriole previously dilated by systemic hypoxia induced a vasoconstriction. However, no arteriolar constriction was observed when a puff was applied to an arteriole after branch vein occlusion.
These results show that experimental branch vein occlusion induces in the affected retina an impairment in the release of constitutive NO and an arteriolar constriction, which, in turn, contributes to the development of hypoxia in tissue and neuronal swelling and death in the inner retina.
视网膜分支静脉阻塞（BVO）后，穿过阻塞区域的小动脉常发生收缩。这种收缩可持续数周，并与未灌注毛细血管扩展区域的形成相关。这些是一项研究的结果，支持了一氧化氮（NO）生成减少导致观察到的小动脉收缩这一假说。
在麻醉的小型猪中，于实验性分支静脉阻塞前及阻塞后的最初4小时内，使用NO微探针测量视网膜前[NO]。小动脉直径的变化与视网膜前[NO]的变化相关。在全身缺氧和分支静脉阻塞后，通过视网膜前微量注射硝基-L-精氨酸（L-NA）来检测视网膜小动脉对内源性NO的敏感性。
分支静脉阻塞后2小时，视网膜前[NO]下降73.7±4%，同时受累区域小动脉直径下降25.4±3.4%。两者在分支静脉阻塞后至少持续4小时。向先前因全身缺氧而扩张的小动脉微量注射L-NA可诱导血管收缩。然而，在分支静脉阻塞后向小动脉微量注射L-NA时，未观察到小动脉收缩。
这些结果表明，实验性分支静脉阻塞在受累视网膜中诱导内源性NO释放受损和小动脉收缩，进而导致组织缺氧以及视网膜内层神经元肿胀和死亡。
