Spasm of the coronary arteries: causes and consequences (the scientist's viewpoint).
Spasm of the coronary arteries: causes and consequences (the scientist's viewpoint).
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冠状动脉痉挛：原因和后果（科学家的观点）。
DOI：
10.1016/s0025-6196(12)65280-x
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发表时间：
1985
影响因子：
8.9
通讯作者：
Vanhoutte,PM
中科院分区：
文献类型：
--
作者：
Shepherd,JT;Vanhoutte,PM
β1-和α1-肾上腺素受体均存在于犬冠状动脉，它们可被交感神经释放的去甲肾上腺素所吸收。在正常情况下，这些动脉因β1-肾上腺素受体的优势而松弛，而在β1-肾上腺素受体拮抗剂存在时，这些动脉则普遍收缩。冠状动脉也有胆碱能神经。当被激活时，这些神经释放乙酰胆碱，乙酰胆碱作用于交感神经末梢的毒蕈碱受体，减少去甲肾上腺素的输出，从而减轻β1-肾上腺素受体介导的松弛。因此，毒蕈碱激动剂可引起冠状动脉痉挛。如果冠状动脉的平滑肌细胞缺氧，它们对β-肾上腺素能刺激的反应丧失，收缩反应被夸大。心脏糖苷阻止去甲肾上腺素的β-肾上腺素能作用的优势。因此，在用瓦巴因治疗后，从交感神经释放去甲肾上腺素不会导致松弛，而是导致冠状动脉进一步收缩。冠状动脉内皮通过前列环素的形成和释放抑制血小板聚集，并通过引起下层平滑肌的松弛而对血小板产物起反应。此外，如果形成凝血酶，也会引起内皮介导的松弛。如果内皮受损，这些保护机制就会丧失。冠状动脉痉挛患者通常在痉挛部位的动脉有形态学改变。血小板可以聚集在这个位置并释放血管活性物质，这有助于形成凝血酶引起收缩。因此，心肌的血液供应减少；随之而来的缺氧加剧了收缩。冠状血管痉挛引起的急性心肌缺血可引起急性心律失常和室性心动过速或心房颤动引起的猝死。
Both β1- and α1-adrenoceptors are present on canine coronary arteries, and they are accessible to norepinephrine released from the sympathetic nerves. Under normal conditions, these arteries relax because of the predominance of the β1-adrenoceptors, whereas constriction prevails in the presence of β1-adrenoceptor antagonists. The coronary arteries also have cholinergic nerves. When activated, these nerves release acetylcholine, which acts on muscarinic receptors on the sympathetic nerve terminals to reduce the output of norepinephrine and thereby lessen the relaxation mediated by β1-adrenoceptors. Thus, muscarinic agonists can precipitate coronary artery spasm. If the smooth muscle cells of the coronary arteries become hypoxic, their responsiveness to β-adrenergic stimulation is lost and constrictor responses are exaggerated. Cardiac glycosides prevent the predominance of the β-adrenergic effects of norepinephrine. Therefore, after treatment with ouabain, release of norepinephrine from the sympathetic nerves leads not to relaxation but to further contraction of coronary arteries. The endothelium of the coronary arteries inhibits platelet aggregation by the formation and release of prostacyclin, and it reacts to platelet products by causing relaxation of the underlying smooth muscle. In addition, if any thrombin is formed, it also causes endothelium-mediated relaxation. If the endothelium is damaged, these protective mechanisms are lost. Patients with coronary artery spasm usually have morphologic changes in the artery at the site of the spasm. Platelets can aggregate at this site and release vasoactive substances, which—aided by formation of thrombin—cause contraction. Thus, the blood supply to the myocardium is reduced; the ensuing hypoxia augments the constriction. Acute myocardial ischemia caused by coronary vasospasm may precipitate acute cardiac rhythm disturbances and sudden death by ventricular tachycardia or fibrillation.