Schultz H D
Department of Physiology and Biophysics, University of Nebraska College of Medicine, Omaha, Nebraska 68198-4575, USA.
Ann N Y Acad Sci. 2001 Jun;940:59-73.
Stimulation of cardiac vagal afferent endings evokes reflex hypotension and bradycardia, also known as a Bezold-Jarisch effect. The physiological importance of this reflex pathway remains uncertain today, but it is increasingly apparent that cardiac vagal afferents can play an important role in modulating cardiovascular control in pathophysiological states, particularly myocardial ischemia. The afferent endings that compose this vagal input are functionally diverse. Ventricular endings exist that are stimulated by wall motion. However, cardiac chemosensitive endings, stimulated by a variety of metabolically active substances known to be produced by the stressed myocardium (e.g., bradykinin, prostaglandins, reactive oxygen species), play a major role in mediating reflex adjustments during myocardial ischemia. Data are presented highlighting the importance of arachidonic acid metabolites and oxygen radicals in activating cardiac vagal endings during myocardial ischemia and reperfusion, and their role in modulating cardiac afferent sensitivity in the disease states of heart failure and insulin-dependent diabetes.
刺激心脏迷走神经传入末梢会引发反射性低血压和心动过缓,也称为贝佐尔德-雅里什效应。如今,这条反射通路的生理重要性仍不确定,但越来越明显的是,心脏迷走神经传入在病理生理状态下,尤其是心肌缺血时,对调节心血管控制可发挥重要作用。构成这种迷走神经传入的传入末梢在功能上具有多样性。存在受心室壁运动刺激的心室末梢。然而,受应激心肌产生的多种代谢活性物质(如缓激肽、前列腺素、活性氧)刺激的心脏化学敏感末梢,在介导心肌缺血期间的反射调节中起主要作用。本文提供的数据突出了花生四烯酸代谢产物和氧自由基在心肌缺血和再灌注期间激活心脏迷走末梢中的重要性,以及它们在心力衰竭和胰岛素依赖型糖尿病等疾病状态下调节心脏传入敏感性中的作用。