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一氧化氮在冠状动脉血管运动中的作用以及冠状动脉粥样硬化及其风险的影响。

Role of nitric oxide in coronary arterial vasomotion and the influence of coronary atherosclerosis and its risks.

作者信息

Goodhart D M, Anderson T J

机构信息

Department of Medicine, University of Calgary, Alberta, Canada.

出版信息

Am J Cardiol. 1998 Nov 1;82(9):1034-9. doi: 10.1016/s0002-9149(98)00550-5.

DOI:10.1016/s0002-9149(98)00550-5
PMID:9817477
Abstract

Healthy coronary vascular endothelium releases nitric oxide to modulate resting and dynamic coronary arterial tone. We studied the impact of atherosclerosis and/or its risks on endothelial nitric oxide release in response to metabolic stimuli by evaluating coronary vasomotor responses to atrial pacing before and after the inhibition of nitric oxide production by intracoronary NG-monomethyl-L-arginine (L-NMMA) (20 micromol/min) infusion. The study includes 34 patients (15 with coronary disease, 11 with normal coronary arteries and > or =1 risk factor, and 8 with normal coronary arteries and no risks). Coronary blood flow was derived from Doppler flow velocity (0.018-inch Doppler wire) and coronary diameter. L-NMMA infusion reduced coronary blood flow by 18 +/- 16% and coronary diameter by 10 +/- 9%. Responses were identical in all subgroups. Coronary blood flow responses to pacing were similar in all subgroups and were unaffected by L-NMMA (11 +/- 11 vs 13 +/- 9 ml/min; p = 0.26). Epicardial coronary vasodilation to control pacing occurred in patients with normal coronary arteries with (4.0 +/- 5.2%, p = 0.01) or without (8.0 +/- 5.2%, p = 0.03) risks, but not in patients with coronary disease (2.8 +/- 5.9%). L-NMMA abolished pacing-induced epicardial vasodilation in patients without coronary artery disease, producing a 1.8 +/- 5.1% response, which was similar in all subgroups. We conclude that microvascular responses to rapid atrial pacing are not mediated by nitric oxide. Flow-mediated epicardial coronary arterial responses may be nitric oxide dependent.

摘要

健康的冠状动脉血管内皮会释放一氧化氮来调节静息和动态冠状动脉张力。我们通过评估在冠状动脉内注入N-单甲基-L-精氨酸(L-NMMA,20微摩尔/分钟)抑制一氧化氮生成前后心房起搏时的冠状动脉血管舒缩反应,研究动脉粥样硬化和/或其风险因素对内皮一氧化氮释放及代谢刺激反应的影响。该研究纳入了34例患者(15例患有冠心病,11例冠状动脉正常但有≥1个风险因素,8例冠状动脉正常且无风险因素)。冠状动脉血流量通过多普勒流速(0.018英寸多普勒导丝)和冠状动脉直径得出。注入L-NMMA使冠状动脉血流量减少了18±16%,冠状动脉直径减少了10±9%。所有亚组的反应相同。所有亚组对起搏的冠状动脉血流量反应相似,且不受L-NMMA影响(分别为11±11与13±9毫升/分钟;p = 0.26)。有风险因素(4.0±5.2%,p = 0.01)或无风险因素(8.0±5.2%,p = 0.03)的冠状动脉正常患者,其心外膜冠状动脉对对照起搏出现血管舒张,但冠心病患者未出现(2.8±5.9%)。L-NMMA消除了无冠状动脉疾病患者起搏诱导的心外膜血管舒张,产生了1.8±5.1%的反应,所有亚组情况相似。我们得出结论,微血管对快速心房起搏的反应不是由一氧化氮介导的。血流介导的心外膜冠状动脉反应可能依赖于一氧化氮。

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