Infarct size limitation by preconditioning: its phenomenological features and the key role of adenosine.
Infarct size limitation by preconditioning: its phenomenological features and the key role of adenosine.
复制标题
通过预处理限制梗死面积：其现象学特征和腺苷的关键作用。
DOI：
10.1093/cvr/27.1.36
复制
发表时间：
1993
影响因子：
10.8
通讯作者：
Osamu Iimura
中科院分区：
文献类型：
--
作者：
T. Miura;Osamu Iimura
Tetsuji Miura和Osamu Iimura的术语“预处理”最早由Murry等人以其当前的含义使用，他们发现在随后的较长缺血之前将T心肌暴露于短暂的短暂缺血，矛盾地延迟了较长缺血期间的心肌坏死。他们将这种心脏保护作用称为“预处理”。从那时起，越来越多的证据表明缺血预处理可以显着保护心肌免受各种形式的缺血再灌注损伤，例如缺血性坏死、“缺血后功能障碍”、缺血诱导的心律失常：和再灌注心律失常。”其中，预处理引起的缺血性坏死的延迟是相当惊人和明确的，与迄今为止测试的药理学药物（包括钙拮抗剂和自由基清除剂）获得的相互矛盾的结果相反。本综述的主要目的是总结本实验室的研究，阐明预处理对缺血性心肌坏死的影响和内源性腺苷在其机制中的作用。实验和临床研究的临床意义也进行了简要讨论。
Tetsuji Miura and Osamu Iimura he term “preconditionin was first used in its current meaning by Murry et al, who found that exposing the T myocardium to a brief transient ischaemia prior to a subsequent longer ischaemia paradoxically delayed myocardil necrosis during the longer ischaemia. They termed the cardioprotective effect “preconditioning”.’Ever since, there has been a rapidly growing body of evidence which indicates that ischaemic preconditioning affords marked protection for the myocardium against various forms of ischaemid reperfusion injury, such as ischaemic necrosis,’’postischaemia dysfunction,’ischaemia induced arrhythmia: and reperfusion arrhythmia.’‘Of these, the delay of ischaemic necrosis caused by preconditioning is quite striking and unequivocal, in contrast to the conflicting results achieved with the pharmacological agents tested to date, including calcium antagonists’’and free radical scavengers.’‘‘I The primary objective of this review is to summarise the studies performed in our laboratory that characterise the effect of preconditioning on ischaemic myocardial necrosis and the role of endogenous adenosine in its mechanism. The clinical implications of the experimental and clinical investigations are also briefly discussed.