Baumgart D, Heusch G
Abteilung für Pathophysiologie, Universitätsklinikum Essen, FRG.
Basic Res Cardiol. 1995 Mar-Apr;90(2):142-59. doi: 10.1007/BF00789444.
Controversies on acetylcholine-induced increases or decreases in coronary blood flow arise from obvious species differences, the role of endothelium in mediating vascular smooth muscle responses, and the marked negative chronotropic and inotropic effects of acetylcholine. In man, there appears to be a predominant dilation of intact epicardial coronary arteries and a constriction of artherosclerotic segments. However, at present there is no evidence for a vagal initiation of myocardial ischemia. Coronary vascular beta-adrenergic receptors mediate dilation, but appear to be functionally insignificant during sympathetic activation. The beta-adrenergic mechanism contributing to myocardial ischemia are indirect, mediated by a tachycardia-related redistribution of blood flow away from the ischemic myocardium. alpha-Adrenergic receptors mediating epicardial coronary artery constriction in experimental studies appear not to be responsible for the initiation of ischemia in patients with angina at rest. However, alpha-adrenergic constriction of coronary resistance vessels resulting in the precipitation of post-stenotic myocardial ischemia was demonstrated in experimental studies and recently confirmed in patients with effort angina. Non-adrenergic, non-cholinergic neurotransmitters exist; however, their role in regulating coronary blood flow remains entirely unclear.
关于乙酰胆碱引起冠状动脉血流量增加或减少的争议源于明显的物种差异、内皮在介导血管平滑肌反应中的作用以及乙酰胆碱显著的负性变时和变力作用。在人类中，完整的心外膜冠状动脉似乎主要发生扩张，而动脉粥样硬化节段则发生收缩。然而，目前尚无证据表明迷走神经会引发心肌缺血。冠状动脉血管β-肾上腺素能受体介导血管扩张，但在交感神经激活期间其功能似乎并不重要。导致心肌缺血的β-肾上腺素能机制是间接的，由与心动过速相关的血流从缺血心肌重新分布介导。在实验研究中，介导心外膜冠状动脉收缩的α-肾上腺素能受体似乎与静息性心绞痛患者的缺血起始无关。然而，实验研究表明冠状动脉阻力血管的α-肾上腺素能收缩会导致狭窄后心肌缺血的发生，最近在劳力性心绞痛患者中也得到了证实。存在非肾上腺素能、非胆碱能神经递质；然而，它们在调节冠状动脉血流量中的作用仍完全不清楚。
