Edwards R J, Marber M S
Department of Cardiology, United Medical and Dental School of Guy's Hospital, London, UK.
Int J Clin Pract. 1998 Sep;52(6):395-401.
Myocardial preconditioning describes the profound myocardial protection that follows a short episode of sublethal ischaemia. Adenosine is produced in ischaemic myocardium and is thought to be an important trigger of the protective mechanism. The exact pathway awaits full elucidation but activation of G proteins and subsequently protein kinase C appear to be important signals. End effectors responsible for delaying cell death include opening of K+ATP ion channels and the transcription of a family of cytoprotective proteins. Absolute proof that preconditioning occurs in man is still awaited, although cross clamping of the aorta during cardiac surgery, balloon inflation during coronary angioplasty, warm-up angina and preinfarction angina are surrogate models supporting its existence. A clearer understanding of the protective mechanisms involved could lead to the development of novel therapeutic agents that could save the infarcting myocardium.
心肌预处理描述的是短暂亚致死性缺血发作后出现的显著心肌保护作用。腺苷在缺血心肌中产生,被认为是保护机制的重要触发因素。确切途径尚待充分阐明,但G蛋白的激活以及随后蛋白激酶C的激活似乎是重要信号。负责延迟细胞死亡的终效应器包括K+ATP离子通道的开放和一类细胞保护蛋白的转录。尽管心脏手术期间主动脉交叉钳夹、冠状动脉成形术期间球囊扩张、热身性心绞痛和梗死前心绞痛是支持其存在的替代模型,但人类中预处理的确切证据仍有待证实。对所涉及保护机制的更清晰理解可能会促成新型治疗药物的开发,从而挽救梗死心肌。