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急性心肌梗死患者体内内源性阿片肽的血浆水平。

Plasma levels of endogenous opioid peptides in patients with acute myocardial infarction.

作者信息

Chen Y T, Lin C J, Lee A Y

机构信息

Department of Internal Medicine, Taichung Veterans General Hospital, Taiwan, Republic of China.

出版信息

Jpn Heart J. 1995 Jul;36(4):421-7. doi: 10.1536/ihj.36.421.

Abstract

There is substantial evidence that cardiac opioid receptors are activated during arrhythmias induced by administration of opioid peptides or myocardial ischemia, supporting the hypothesis that endogenous opioid peptides (EOP) are involved in myocardial infarction. This prospective clinical trial is designed to determine whether the ischemia-induced arrhythmias and extent of the infarct are related to the release of the EOP beta-endorphin in patients with acute myocardial infarction. Two groups were included in the study, patients with acute myocardial infarction, and healthy volunteers who served as controls. The results indicate that, compared to the controls, there was augmentation of ischemic arrhythmias and ischemic damage as assessed by serum creatine kinase activity, accompanied by an elevated level of beta-endorphin, in patients with acute myocardial infarction. The above data strongly indicate that EOP are indeed involved in the pathophysiology of myocardial infarction, and suggest these peptides have an important role in ischemic heart disease.

摘要

有大量证据表明,在给予阿片肽或心肌缺血诱导的心律失常过程中,心脏阿片受体被激活,这支持了内源性阿片肽(EOP)参与心肌梗死的假说。这项前瞻性临床试验旨在确定急性心肌梗死患者缺血诱导的心律失常和梗死范围是否与EOPβ-内啡肽的释放有关。研究纳入了两组,急性心肌梗死患者和作为对照的健康志愿者。结果表明,与对照组相比,急性心肌梗死患者缺血性心律失常增加,血清肌酸激酶活性评估的缺血损伤加重,同时β-内啡肽水平升高。上述数据有力地表明,EOP确实参与了心肌梗死的病理生理学过程,并提示这些肽在缺血性心脏病中起重要作用。

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