Grimm D R
Spinal Cord Damage Research Center, Veterans Affairs Medical Center, Bronx, New York 10468, USA.
J Clin Neurophysiol. 1997 May;14(3):170-82. doi: 10.1097/00004691-199705000-00002.
This article reviews the basic physiology of the reflexogenic areas of the heart and the mechano- and baroreceptors that regulate cardiovascular and autonomic homeostasis, all of which contribute to our understanding of the pathogenesis of neurally mediated syncope. The mechanisms of neurally mediated syncope may involve excessive activation of ventricular receptors that trigger severe hypotension and bradycardia. Thus, neurally mediated syncope may be the clinical expression of the Bezold-Jarisch reflex, which occurs in situations of increased sympathetic activity, perhaps as a result of heightened cardiac receptor sensitivity. The arterial baroreceptors exert a ubiquitous influence on the heart and circulation, and serve primarily to buffer transient changes in arterial pressure by transmitting sensory information regarding their stretch to the central nervous system. This information, in conjunction with cardiac receptor input, elicits alterations in neural efferent output from sympathetic and parasympathetic fibers to provide subtle, continuous regulation of beat-to-beat cardiovascular hemodynamics to an array of physiologic and psychological stressors.
本文回顾了心脏反射区的基本生理学以及调节心血管和自主神经稳态的机械感受器和压力感受器,所有这些都有助于我们理解神经介导性晕厥的发病机制。神经介导性晕厥的机制可能涉及心室感受器的过度激活,从而引发严重的低血压和心动过缓。因此,神经介导性晕厥可能是贝佐尔德-雅里什反射的临床表现,该反射发生在交感神经活动增加的情况下,可能是由于心脏感受器敏感性增强所致。动脉压力感受器对心脏和循环系统具有广泛影响,主要通过将有关其牵张的感觉信息传递到中枢神经系统来缓冲动脉压力的瞬时变化。这些信息与心脏感受器的输入相结合,引发交感神经和副交感神经纤维神经传出输出的改变,从而对一系列生理和心理应激源进行逐搏心血管血流动力学的精细、持续调节。