Purpose: The development of extended areas of nonperfused capillaries after branch vein occlusion (BVO) is correlated to the secondary constriction of the arteriole crossing the occluded area. The decrease in nitric oxide (NO) in tissue that occurs early after BVO accounts for the secondary arteriolar constriction. The present study shows that the administration of an NO donor can reverse the secondary arteriolar vasoconstriction observed after BVO.
Methods: Simultaneous preretinal NO profiles and arteriolar diameter measurements were performed in miniature pigs after experimental BVO. The effect of preretinal microinjections of the NO donor sodium nitroprusside (SNP) on the arteriolar diameter was studied.
Results: Significant arteriolar vasoconstriction (mean arteriolar diameter, 92.1% +/- 3.3% of control; n = 7; P = 7.4 x 10(-5)) and a simultaneous decrease in the preretinal NO concentration ([NO]) (preretinal [NO], 20% +/- 15.6% of control; n = 5; P = 0.0003) were observed 4 hours after BVO. Microinjection of the NO donor SNP (1 mM applied by puffer) near the constricted retinal arteriole caused a segmental, reversible arteriolar dilation that reached its maximum 20 minutes after the injection (mean arteriolar diameter; 110.8% +/- 7.5% of control; n = 6; P = 0.02) and was completely reversed 60 minutes later (n = 6).
Conclusions: Local administration of NO donors may contribute to the restoration of the retinal arteriolar blood flow after BVO and thus may improve the supply of oxygen and nutrients to the injured tissue.
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