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Mechanisms of Cardioprotection Against Ischemia Reperfusion injury

机译:心脏应激对缺血再灌注损伤的机制

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Summary. The high incidence of morbidity and mortality associated with acute myocardial ischemia (AMI) has stimulated substantial research to salvage the dying myocardium. Early restoration of flow to the ischemic myocardium by different interventions has significantly reduced the mortality associated with the acute coronary syndrome but could not improve the morbidity. Accordingly, the possibility of reperfusion injury, and not ischemic injury, as the cause of post ischemic myocardial dysfunction is being considered seriously. Ventricular arrhythmias, myocardial stunning and cell death are the prominent sequels to post ischemic reperfusion. Although thrombolytic and other therapies Eke percutaneous transluminal angio-plasty and coronary artery bypass grafting have "significantly increased the rate of survival of AMI patients, these procedures have also spurred interest in the phenomena of ischemia reperfusion injury. In view of the immense clinical consequences of ischemia reperfusion in humans, a large number of animal studies have been carried out to understand the patho-physiology and therapy. This article elaborates different mechanisms which have been suggested to cause ischemia reperfusion injury'as well as therapeutic modalities that have shown promise in reducing the associated cardiac abnormalities.
机译:概括。发病率和急性心肌缺血(AMI)相关的死亡率高发的刺激大量研究以挽救濒死心肌。通过不同的干预流向心肌缺血的早期恢复已显著降低与急性冠脉综合征相关的死亡率,但不能提高发病率。因此,再灌注损伤,而不是缺血性损伤,为缺血后心肌功能障碍的原因的可能性正在认真考虑。室性心律失常,心肌顿抑和细胞死亡是突出续集缺血后再灌注。虽然在缺血再灌注损伤的现象溶栓等治疗勉强维持经皮腔内血管成形术和冠状动脉旁路移植术已经“显著上升的急性心肌梗死患者的成活率,这些程序也刺激了兴趣。鉴于的巨大临床后果在人类缺血再灌注损伤,大量动物研究已经进行了了解病理生理学和治疗。本文论述已建议引起缺血再灌注injury'as以及治疗方式的不同机制,在减少显露才华相关的心脏异常。

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