Schmetterer L, Krejcy K, Kastner J, Wolzt M, Gouya G, Findl O, Lexer F, Breiteneder H, Fercher A F, Eichler H G
Department of Clinical Pharmacology, University of Vienna, Austria.
Exp Eye Res. 1997 Mar;64(3):305-12. doi: 10.1006/exer.1996.0213.
There is experimental evidence that endothelium derived nitric oxide is involved in the regulation of ocular vascular tone. The purpose of this study was to investigate the effects of NO-synthase inhibition by N-monomethyl-L-arginine (L-NMMA) on ocular fundus pulsations in young healthy volunteers. Three milligrams per kilograms L-NMMA were administered i.v. over 5 minutes. Protocol 1: Measurements of blood pressure, pulse rate, fundus pulsation amplitude, NO-exhalation, and cardiac output were performed at baseline and 10, 30, 60, 90, 150, and 300 minutes after L-NMMA infusion (n = 8). Fundus pulsation amplitude, which has been shown to estimate the pulsatile component of the choroidal blood flow, was recorded with a recently developed laser interferometer. Protocol 2: Measurements of blood pressure, pulse rate, fundus pulsation amplitude, NO-exhalation, and blood flow velocity in the ophthalmic artery were performed in a randomized, placebo controlled cross over study (n = 10). Ten minutes after L-NMMA administration fundus pulsation amplitude decreased by 23 +/- 2% (protocol 1) and 19 +/- 1% (protocol 2, P < 0.01 each), cardiac output by 12 +/- 2% (P < 0.01), and exhaled NO by 55 +/- 6% (protocol 1) and 41 +/- 6% (protocol 2, P < 0.01 each). All parameters returned to baseline values within the 300 minutes observation period, with a faster recovery of fundus pulsation amplitude than of cardiac output and exhaled NO. Blood pressure, pulse rate, and ophthalmic artery blood flow velocity showed only minor changes during and after administration of L-NMMA. Our results suggest that systemic NO-synthase inhibition reduces pulsatile choroidal and most likely total choroidal blood flow in humans. The recovery of vascular tone in choroidal vessels seems to be different from the cardiovascular response. Our findings indicate that reduced fundus pulsations after L-NMMA are caused by systemic factors as well as by local reactions of the choroidal vasculature.
有实验证据表明，内皮衍生的一氧化氮参与眼血管张力的调节。本研究的目的是调查N-单甲基-L-精氨酸（L-NMMA）抑制一氧化氮合酶对年轻健康志愿者眼底搏动的影响。以每千克3毫克的剂量静脉注射L-NMMA，持续5分钟。方案1：在基线以及L-NMMA输注后10、30、60、90、150和300分钟测量血压、脉搏率、眼底搏动幅度、一氧化氮呼出量和心输出量（n = 8）。眼底搏动幅度已被证明可用于估计脉络膜血流的搏动成分，使用最近开发的激光干涉仪进行记录。方案2：在一项随机、安慰剂对照的交叉研究中（n = 10）测量血压、脉搏率、眼底搏动幅度、一氧化氮呼出量和眼动脉血流速度。给予L-NMMA 10分钟后，眼底搏动幅度下降了23±2%（方案1）和19±1%（方案2，均P < 0.01），心输出量下降了12±2%（P < 0.），呼出的一氧化氮下降了55±6%（方案1）和41±6%（方案2，均P < 0.01）。在300分钟的观察期内，所有参数均恢复到基线值，眼底搏动幅度的恢复比心输出量和呼出的一氧化氮更快。在给予L-NMMA期间和之后，血压、脉搏率和眼动脉血流速度仅显示出轻微变化。我们的结果表明，全身性一氧化氮合酶抑制会降低人类脉络膜的搏动性血流，很可能还会降低脉络膜的总血流量。脉络膜血管张力的恢复似乎与心血管反应不同。我们的研究结果表明，L-NMMA后眼底搏动减少是由全身因素以及脉络膜血管系统的局部反应引起的。
