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论心肌缺血的成因

On the genesis of myocardial ischemia.

作者信息

Sroka K

机构信息

Stellinger Weg 47, 20255 Hamburg, Germany.

出版信息

Z Kardiol. 2004 Oct;93(10):768-83. doi: 10.1007/s00392-004-0137-6.

Abstract

About three quarters of myocardial ischemic events are triggered by the autonomic nervous system. The pathognomonic constellation is a combination of an almost complete withdrawal of tonic vagal activity with increased sympathetic activity. The reduction of tonic vagal activity, which is characteristic for ischemic heart disease, and the acute withdrawal of vagal drive preceding the onset of ischemia are not dependent on coronary artery disease. In this paper, the pathophysiological steps that lead from sympathetic-parasympathetic imbalance to myocardial ischemia shall be discussed. A considerable increase of aerobic glycolysis within the myocardium as a result of the autonomic imbalance is of special importance in this process.

摘要

大约四分之三的心肌缺血事件是由自主神经系统触发的。典型症状是迷走神经张力活动几乎完全减退并伴有交感神经活动增加。缺血性心脏病的特征性表现是迷走神经张力活动减退,以及缺血发作前迷走神经驱动的急性减退,这与冠状动脉疾病无关。本文将讨论从交感-副交感神经失衡导致心肌缺血的病理生理过程。在这一过程中,自主神经失衡导致心肌内有氧糖酵解显著增加具有特别重要的意义。

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