Baker Christopher S R, Kumar Sanjay, Rimoldi Ornella E
MRC Clinical Sciences Center and National Heart & Lung Institute, Faculty of Medicine, Imperial College School of Science, Technology and Medicine, Hammersmith Hospital, London, UK.
Heart Fail Rev. 2003 Apr;8(2):127-41. doi: 10.1023/a:1023088601481.
Brief myocardial ischemia/reperfusion has complex effects on the myocardium. In the short term the myocardium may be stunned with temporarily reduced contractile function, though this may also be accompanied by the modification and de novo synthesis of proteins that protect the heart against subsequent early or delayed insults. Repeated episodes of non-lethal ischemia, which are common in the clinical setting, combine all of these phenomena and may ultimately result in chronic contractile dysfunction. Nitric oxide is intimately linked to many of these alterations in cellular function and defense. This article examines data predominantly from in vivo large animal studies that relate to these ischemia-induced changes, the evidence for the proposed mechanisms behind both myocardial stunning and preconditioning while concentrating on the role of nitric oxide in these conditions.
短暂性心肌缺血/再灌注对心肌有复杂的影响。短期内,心肌可能会出现顿抑,收缩功能暂时降低,不过这也可能伴随着蛋白质的修饰和从头合成,这些蛋白质可保护心脏免受随后的早期或延迟性损伤。在临床环境中常见的非致死性缺血反复发作,会综合所有这些现象,并最终可能导致慢性收缩功能障碍。一氧化氮与细胞功能和防御中的许多这些改变密切相关。本文主要研究来自体内大型动物研究的数据,这些数据与这些缺血诱导的变化、心肌顿抑和预处理背后的拟议机制的证据相关,同时重点关注一氧化氮在这些情况下的作用。