Nitric oxide activity is deficient in spasm arteries of patients with coronary spastic angina
Nitric oxide activity is deficient in spasm arteries of patients with coronary spastic angina
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DOI：
10.1161/01.cir.94.3.266
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发表时间：
1996-08-01
期刊：
影响因子：
37.8
通讯作者：
Kawano, H
中科院分区：
文献类型：
--
作者：
Kugiyama, K;Yasue, H;Kawano, H
研究背景：乙酰胆碱、5-羟色胺、麦角新碱或组胺均可引起冠状动脉痉挛，当内皮细胞完整时，这些物质均可通过释放一氧化氮（NO）引起血管舒张。硝酸甘油通过转化为NO使血管扩张，从而迅速缓解冠状动脉痉挛。因此，冠状动脉痉挛性心绞痛（CSA）患者痉挛动脉中NO释放可能不足。本研究的目的是确定是否NO释放不足，在冠状动脉的患者CSA.Methods和结果N-G-单甲基-L-精氨酸（L-NMMA），一种NO合成酶的抑制剂，注入冠状动脉痉挛性心绞痛（CSA）患者21例，并在28名对照患者。冠状动脉痉挛是由冠状动脉内注射乙酰胆碱引起的，并在所有CSA患者中通过血管造影记录。L-NMMA剂量依赖性地降低对照组患者冠状动脉的基底管腔直径，而对CSA患者痉挛动脉的基底直径无影响。L-NMMA可抑制对照动脉对乙酰胆碱的扩张反应，增强收缩反应，而对痉挛动脉对乙酰胆碱的收缩反应无影响。冠状动脉内输注L-精氨酸不影响痉挛或控制动脉的直径。与对照动脉相比，痉挛动脉对硝酸甘油的扩张反应明显增加，而对地尔硫卓的反应没有差异themes.Conclusions痉挛动脉中内皮NO活性不足，导致CSA患者动脉对硝酸甘油的血管扩张作用和乙酰胆碱的血管收缩作用超敏感。这种内皮NO活性的缺乏在冠状动脉痉挛的发病机制中起重要作用。
Background Coronary spasm can be induced by acetylcholine, serotonin, ergonovine, or histamine, all of which cause vasodilation when the endothelium is intact by releasing nitric oxide (NO). Coronary spasm is promptly relieved by nitroglycerin, which vasodilates through its conversion to NO. It is thus possible that NO release may be deficient in the spasm arteries in patients with coronary spastic angina (CSA). The aim of this study was to determine whether NO release is deficient in coronary arteries of patients with CSA.Methods and Results N-G-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthase, was infused into coronary arteries in 21 patients with coronary spastic angina (CSA) and in 28 control patients. Coronary spasm was induced by intracoronary injection of acetylcholine and was documented angiographically in all patients with CSA. L-NMMA dose-dependently decreased basal luminal diameter of coronary arteries in control patients, whereas it had no effect on basal diameter of the spasm arteries in patients with CSA. L-NMMA abolished the dilator response to acetylcholine and enhanced the constrictor response to acetylcholine in control arteries, whereas it had no effect on the constrictor response to acetylcholine in spasm arteries. Intracoronary infusion of L-arginine did not affect the diameter of spasm or control arteries. The dilator response to nitroglycerin was increased markedly in spasm arteries compared with control arteries, whereas response to diltiazem did not differ between them.Conclusions There is a deficiency in endothelial NO activity in spasm arteries, which leads to the supersensitivity of the artery to the vasodilator effect of nitroglycerin and to the vasoconstrictor effect of acetylcholine in patients with CSA. This deficient endothelial NO activity plays an important role in the pathogenesis of coronary spasm.