Krajcar M, Heusch G
Abteilung für Pathophysiologie, Universitätsklinikum Essen.
Basic Res Cardiol. 1993;88 Suppl 1:25-42. doi: 10.1007/978-3-642-72497-8_3.
The powerful local metabolic regulation adjusting coronary blood flow to myocardial oxygen consumption under normal conditions is beyond doubt. However, despite substantial experimental efforts the responsible mediators are still largely unknown. Adenosine, a purported mediator of local metabolic control of coronary blood flow, is probably only involved in transient flow adaptations, but not in steady-state coronary autoregulation. Even below the autoregulatory range a substantial vasodilator reserve persists. Recruitment of such vasodilator reserve results in improved regional myocardial blood flow and attenuated regional ischemic dysfunction. beta-adrenergic coronary dilation is of minor functional importance. alpha-adrenergic coronary constriction acts to attenuate increases in coronary blood flow during sympathetic activation under normal conditions, such that myocardial oxygen extraction increases to match the increased oxygen consumption. alpha-adrenergic coronary constriction remains operative in ischemic myocardium, thus precipitating or contributing to acute myocardial ischemia during sympathetic activation and exercise in experimental animals as well as in patients with stable angina. The vagal transmitter acetylcholine--upon exogenous intracoronary infusion--induces critical constriction of epicardial coronary arteries with endothelial dysfunction and atherosclerosis. However, a vagal initiation of coronary spasm or myocardial ischemia has not been documented so far. Similarly, peptide hormones/transmitters such as NPY, vasopressin, and angiotensin can induce myocardial ischemia upon exogenous administration. Their pathophysiological role in myocardial ischemia and reperfusion, however, remains to be established.
在正常情况下，强大的局部代谢调节可使冠状动脉血流与心肌耗氧量相匹配，这一点毋庸置疑。然而，尽管进行了大量实验研究，但起作用的介质仍大多未知。腺苷被认为是冠状动脉血流局部代谢控制的介质，可能仅参与短暂的血流适应，而不参与冠状动脉的稳态自动调节。即使在自动调节范围以下，仍存在大量的血管舒张储备。启用这种血管舒张储备可改善局部心肌血流并减轻局部缺血性功能障碍。β肾上腺素能冠状动脉扩张的功能重要性较小。α肾上腺素能冠状动脉收缩在正常情况下可减弱交感神经激活期间冠状动脉血流的增加，从而使心肌氧摄取增加以匹配增加的氧消耗。α肾上腺素能冠状动脉收缩在缺血心肌中仍然起作用，因此在实验动物以及稳定型心绞痛患者的交感神经激活和运动期间会引发或促成急性心肌缺血。迷走神经递质乙酰胆碱——在冠状动脉内注入外源性乙酰胆碱后——可导致内皮功能障碍和动脉粥样硬化的冠状动脉临界收缩。然而，迄今为止尚未记录到迷走神经引发的冠状动脉痉挛或心肌缺血。同样，肽类激素/递质如神经肽Y、血管加压素和血管紧张素在外源性给药后可诱发心肌缺血。然而，它们在心肌缺血和再灌注中的病理生理作用仍有待确定。
