原文：
A series of brief coronary artery reperfusions and reocclusions applied during the early minutes of coronary artery reflow ("postconditioning") attenuates reperfusion injury. However, it is not known whether brief ischemia-reperfusion applied to a distant organ at the onset of myocardial reperfusion (i.e. "remote postconditioning", remote PostC) reduces infarct size in the reperfused myocardium. In an in vivo anesthetized rat model of myocardial infarction induced by coronary artery occlusion and reperfusion, this study tested the hypothesis that remote postC induced by a single 5 minute episode of renal artery (RA) occlusion and reperfusion applied immediately before the onset of coronary artery reperfusion protects the myocardium from reperfusion injury by mechanisms involving endogenous adenosine receptor activation.
Remote renal postconditioning applied immediately before the onset of coronary artery reperfusion provides potent myocardial infarct size reduction likely exerted during the first minutes of coronary artery reperfusion. This inter-organ remote postconditioning phenomenon is likely mediated in part by release of adenosine by the ischemic-reperfused kidney and subsequent activation of adenosine receptors.
译文：
冠状动脉回流早期的几分钟内应用一系列短暂冠状动脉再灌注和再闭塞（“后处理”）可降低再灌注损伤。然而，于心肌再灌注开始时在远端器官进行短暂缺血再灌注（如远隔后处理）是否能降低再灌注心肌内的梗塞面积尚不清楚。本研究使用冠状动脉闭塞和再灌注诱导的心肌梗塞体内麻醉大鼠模型检验了下列假说，即冠状动脉再灌注开始前立即应用肾动脉阻塞和再灌注进行5分钟诱导的远隔后处理，可通过激活内源性腺苷受体机制来避免心肌再灌注损伤。
冠状动脉再灌注开始前立即应用远隔肾脏后处理可在冠状动脉再灌注前几分钟内有效降低心肌梗塞面积。这种内部器官远隔后处理现象很可能在一定程度上受缺血再灌注肾脏释放的腺苷进而激活腺苷受体的调控。
查找母语润色产品
立即注册
母语化润色服务
下单注意事项