Resch Hemma, Zawinka Claudia, Weigert Günther, Schmetterer Leopold, Garhöfer Gerhard
Medical University of Vienna [corrected]
Invest Ophthalmol Vis Sci. 2005 Nov;46(11):4275-80. doi: 10.1167/iovs.05-0417.
It has been hypothesized that carbon monoxide (CO) acts as an important vascular paracrine factor and plays a role in blood flow regulation in several tissues. The present study investigated the effect of inhaled CO on retinal and choroidal blood flow.
Fifteen healthy male volunteers were studied in a randomized, double-masked, placebo-controlled design with washout periods of at least 1 week between study days. CO in a dose of 500 ppm or placebo (synthetic air without CO) was inhaled for 60 minutes. Ocular hemodynamics were measured at baseline and at 30 and 60 minutes after start of inhalation. Retinal vessel diameters were measured with a retinal vessel analyzer. RBC velocity was assessed using bidirectional laser Doppler velocimetry. Retinal blood flow was calculated based on retinal vessel diameters and RBC velocity. Fundus pulsation amplitude (FPA) was measured using laser interferometry, and submacular choroidal blood flow using laser Doppler flowmetry.
Breathing of CO significantly increased carboxyhemoglobine, from 1.2 +/- 0.5% to 8.5 +/- 0.9% and 9.4 +/- 0.6% at the two time points, respectively (P < 0.01). The diameter of retinal arteries increased by +3.5 +/- 3.8% and +4.2 +/- 3.9% (P < 0.01) in response to CO inhalation. In retinal veins, CO also induced an increase in diameter of +4.3 +/- 3.0% and +4.8 +/- 5.0%, respectively (P < 0.01). By contrast, placebo did not influence retinal vessel diameter. RBC velocity tended to increase during CO inhalation (+8 +/- 22%), but this effect did not reach the level of significance (P = 0.1). Calculated retinal blood flow increased significantly by +12 +/- 5% (P < 0.02). FPA increased after breathing CO by +20 +/- 20% and +26 +/- 21% at the two time points, respectively (P < 0.01). Subfoveal choroidal blood flow increased by +14 +/- 9% and +15 +/- 9% during breathing of CO (P < 0.01).
This experiment demonstrated that retinal and choroidal blood flow increase during inhalation of CO. Whether this increase is caused by tissue hypoxia or a yet unknown mechanism has to be clarified.
有假说认为一氧化碳（CO）作为一种重要的血管旁分泌因子，在多种组织的血流调节中发挥作用。本研究调查了吸入CO对视网膜和脉络膜血流的影响。
15名健康男性志愿者参与研究，采用随机、双盲、安慰剂对照设计，研究日之间的洗脱期至少为1周。吸入剂量为500 ppm的CO或安慰剂（不含CO的合成空气）60分钟。在基线以及吸入开始后30分钟和60分钟测量眼部血流动力学。用视网膜血管分析仪测量视网膜血管直径。使用双向激光多普勒测速仪评估红细胞速度。根据视网膜血管直径和红细胞速度计算视网膜血流量。用激光干涉测量法测量眼底搏动幅度（FPA），用激光多普勒血流仪测量黄斑下脉络膜血流量。
吸入CO后，羧基血红蛋白显著增加，在两个时间点分别从1.2±0.5%增至8.5±0.9%和9.4±0.6%（P<0.01）。吸入CO后，视网膜动脉直径分别增加了+3.5±3.8%和+4.2±3.9%（P<0.01）。在视网膜静脉中，CO也分别使直径增加了+4.3±3.0%和+4.8±5.0%（P<0.01）。相比之下，安慰剂对视网膜血管直径没有影响。吸入CO期间红细胞速度有增加趋势（+8±22%），但这种影响未达到显著水平（P = 0.1）。计算得出的视网膜血流量显著增加了+12±5%（P<0.02）。吸入CO后，两个时间点的FPA分别增加了+20±20%和+26±21%（P<0.01）。吸入CO期间，黄斑下脉络膜血流量增加了+14±9%和+15±9%（P<0.01）。
本实验表明吸入CO期间视网膜和脉络膜血流增加。这种增加是由组织缺氧还是一种未知机制引起，还有待阐明。
