Heusch G, Baumgart D, Camici P, Chilian W, Gregorini L, Hess O, Indolfi C, Rimoldi O
Abteilung für Pathophysiologie and Abteilung für Kardiologie, Universitätsklinikum Essen, Essen, Germany.
Circulation. 2000 Feb 15;101(6):689-94. doi: 10.1161/01.cir.101.6.689.
The use of quantitative coronary angiography, combined with Doppler and PET, has recently been directed at the study of alpha-adrenergic coronary vasomotion in humans. Confirming prior animal experiments, there is no evidence of alpha-adrenergic coronary constrictor tone at rest. Again confirming prior experiments, responses to alpha-adrenoceptor activation are augmented in the presence of coronary endothelial dysfunction and atherosclerosis, involving both alpha(1)- and alpha(2)-adrenoceptors in epicardial conduit arteries and microvessels. Such augmented alpha-adrenergic coronary constriction is observed during exercise and coronary interventions, and it is powerful enough to induce myocardial ischemia and limit myocardial function. Recent studies indicate a genetic determination of alpha(2)-adrenergic coronary constriction.
定量冠状动脉造影结合多普勒和正电子发射断层扫描技术，最近已用于人类α-肾上腺素能冠状动脉血管运动的研究。正如先前动物实验所证实的，静息时不存在α-肾上腺素能冠状动脉收缩张力。再次证实先前的实验，在存在冠状动脉内皮功能障碍和动脉粥样硬化的情况下，对α-肾上腺素能受体激活的反应增强，涉及心外膜传导动脉和微血管中的α(1)和α(2)肾上腺素能受体。这种增强的α-肾上腺素能冠状动脉收缩在运动和冠状动脉介入过程中均可观察到，其强度足以诱发心肌缺血并限制心肌功能。最近的研究表明α(2)肾上腺素能冠状动脉收缩存在遗传决定因素。
