Kalsner S
Department of Physiology, City University of New York Medical School, New York City 10031, USA.
Biochem Pharmacol. 1995 Mar 30;49(7):859-71. doi: 10.1016/0006-2952(94)00447-t.
Myocardial infarction and sudden cardiac death may be initiated by a sudden intense localized contraction of coronary artery smooth muscle. When this event occurs around a vulnerable eccentric lipid-filled plaque, rupture and extrusion of plaque contents and exposure of collagen occur. This may sometimes be a silent and self-limiting event; other times it leads to thrombus formation. A second wave of spasm due to accumulated platelet and inflammatory mediators may compound the contractile consequences of the initiating event. Spasm involves intrinsic smooth muscle cell electrical mechanisms, hyper-responsive cells, and multiple agonists that synergize their actions, and the involvement of each mechanism varies at different times in the sequence of vascular occlusion. Study of spasm requires vascular systems that adequately model coronary artery responses of the ageing human heart. As previously emphasized, tissues obtained postmortem, and when possible from recipients during heart transplants, must be integral to theory building, alongside animal models, despite the experimental limitations such tissues impose. A multidisciplinary approach, at all levels of vascular physiology and pharmacology, will be necessary to understand coronary motor activity and human heart disease.
心肌梗死和心源性猝死可能由冠状动脉平滑肌突然强烈的局部收缩引发。当此事件发生在易损的偏心脂质填充斑块周围时，斑块内容物会破裂和挤出，胶原蛋白暴露。这有时可能是一个无症状且自限性的事件；其他时候则会导致血栓形成。由于血小板和炎症介质积累引起的第二轮痉挛可能会加剧起始事件的收缩后果。痉挛涉及平滑肌细胞的内在电机制、高反应性细胞以及协同作用的多种激动剂，并且每种机制在血管闭塞过程中的不同时间其参与程度各异。对痉挛的研究需要能够充分模拟老年人心脏冠状动脉反应的血管系统。如前所述，尽管此类组织存在实验局限性，但死后获取的组织以及尽可能在心脏移植过程中从受者获取的组织，必须与动物模型一起成为理论构建不可或缺的部分。要理解冠状动脉运动活性和人类心脏病，在血管生理学和药理学的各个层面采用多学科方法将是必要的。
