Inhaled carbon monoxide increases retinal and choroidal blood flow in healthy humans

被引:35
作者
Resch, H
Zawinka, C
Weigert, G
Schmetterer, L
Garhöfer, G
机构
[1] Univ Vienna, Dept Clin Pharmacol, A-1090 Vienna, Austria
[2] Univ Vienna, Ctr Biomed Engn & Phys, A-1090 Vienna, Austria
[3] Univ Vienna, Dept Ophthalmol, A-1090 Vienna, Austria
关键词
D O I
10.1167/iovs.05-0417
中图分类号
R77 [眼科学];
学科分类号
100212 ;
摘要
PURPOSE. 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. METHODS. 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. RESULTS. Breathing of CO significantly increased carboxyhemoglobine, from 1.2 +/-5% to 8.5 +/-9% and 9.4 +/-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 (+ +/- 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). CONCLUSIONS. 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.
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页码:4275 / 4280
页数:6
相关论文
共 48 条
[1]  
BONNER R, 1990, DEV CARDIOVASC MED, P17
[2]   VASCULAR SMOOTH-MUSCLE CELL HEME OXYGENASES GENERATE GUANYLYL CYCLASE STIMULATORY CARBON-MONOXIDE [J].
CHRISTODOULIDES, N ;
DURANTE, W ;
KROLL, MH ;
SCHAFER, AI .
CIRCULATION, 1995, 91 (09) :2306-2309
[3]   CHOROIDAL BLOOD-FLOW .3. EFFECTS OF OXYGEN AND CARBON-DIOXIDE [J].
FRIEDMAN, E ;
CHANDRA, SR .
ARCHIVES OF OPHTHALMOLOGY, 1972, 87 (01) :70-&
[4]   Human skeletal muscle sympathetic nerve activity, heart rate and limb haemodynamics with reduced blood oxygenation and exercise [J].
Hanada, A ;
Sander, M ;
González-Alonso, J .
JOURNAL OF PHYSIOLOGY-LONDON, 2003, 551 (02) :635-647
[5]   Neural circulatory responses to carbon monoxide in healthy humans [J].
Hausberg, M ;
Somers, VK .
HYPERTENSION, 1997, 29 (05) :1114-1118
[6]   Ocular vasodynamic changes in light and darkness in smokers [J].
Havelius, U ;
Hansen, F .
INVESTIGATIVE OPHTHALMOLOGY & VISUAL SCIENCE, 2005, 46 (05) :1698-1705
[7]   Correlation of HO-1 expression with onset and reversal of hypoxia-induced vasoconstrictor hyporeactivity [J].
Jernigan, NL ;
O'Donaughy, TL ;
Walker, BR .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2001, 281 (01) :H298-H307
[8]   Heme oxygenase substrates acutely lower blood pressure in hypertensive rats [J].
Johnson, RA ;
Lavesa, M ;
DeSeyn, K ;
Scholer, MJ ;
Nasjletti, A .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 1996, 271 (03) :H1132-H1138
[9]   A HEME OXYGENASE PRODUCT, PRESUMABLY CARBON-MONOXIDE, MEDIATES A VASODEPRESSOR FUNCTION IN RATS [J].
JOHNSON, RA ;
LAVESA, M ;
ASKARI, B ;
ABRAHAM, NG ;
NASJLETTI, A .
HYPERTENSION, 1995, 25 (02) :166-169
[10]   THE ROLE OF AORTIC CHEMORECEPTORS DURING SEVERE CO HYPOXIA [J].
KING, CE ;
CAIN, SM ;
CHAPLER, CK .
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY, 1985, 63 (05) :509-514