van Lieshout J J, Wieling W, Karemaker J M
Cardiovascular Research Institute Amsterdam, Department of Internal Medicine, Academic Medical Centre, The Netherlands.
Pacing Clin Electrophysiol. 1997 Mar;20(3 Pt 2):753-63. doi: 10.1111/j.1540-8159.1997.tb03901.x.
The orthostatic volume displacement associated with the upright position necessitates effective neural cardiovascular modulation. Neural control of cardiac chronotropy and inotropy, and vasomotor tone aims at maintaining venous return, thus opposing gravitational pooling of blood in the lower part of the body. The present concept of the vasovagal response or "common faint" implicates the development of inappropriate cardiac slowing due to sudden augmentation of efferent vagal activity, and arteriolar dilatation by sudden reduction or cessation of sympathetic activity. The venous pooling associated with lasting orthostatic stress results in development of central hypovolemia. At a certain point during the ongoing reflex adaptation to the hypovolemia in progress, a depressor reflex is set in train. The depressor reflex input along this second "peripheral" afferent pathway is postulated to originate from various sites in the cardiovascular system but remains uncertain. The common faint in humans is of both vaso- and vagal origin; the pure vagal response is less common than its vasodepressor variant. There is strong evidence for an early loss of vasomotor tone in the majority of fainting subjects. Blocking the vagus nerve or cardiac pacing is not of much help in preventing vasovagal syncope; though atropine or pacing may prevent bradycardia in vasovagal fainting, they have never been proven to prevent hypotension. Baroreflex modulation of autonomic outflow remains present during the presyncopal stages until it becomes offset by an opposing depressor reflex with relative bradycardia and relaxation of arterial resistance vessels. The nature of the vasodilatation associated with the vasovagal response has still not been settled.
与直立姿势相关的体位性容量移位需要有效的神经心血管调节。对心脏变时性和变力性以及血管舒缩张力的神经控制旨在维持静脉回流，从而对抗血液在身体下部的重力性淤积。目前关于血管迷走神经反应或“普通昏厥”的概念意味着，由于传出迷走神经活动突然增强导致不适当的心脏减慢，以及交感神经活动突然减少或停止导致小动脉扩张。与持续性直立应激相关的静脉淤积会导致中枢性血容量减少。在对正在发生的血容量减少进行持续反射适应的某个阶段，会引发降压反射。沿着这条第二条“外周”传入途径的降压反射输入被认为起源于心血管系统的各个部位，但仍不确定。人类的普通昏厥既有血管源性又有迷走神经源性；纯迷走神经反应比血管减压型变体少见。有强有力的证据表明，大多数昏厥受试者早期会出现血管舒缩张力丧失。阻断迷走神经或心脏起搏对预防血管迷走性晕厥帮助不大；虽然阿托品或起搏可能预防血管迷走性昏厥时的心动过缓，但从未被证明能预防低血压。在晕厥前期，自主神经输出的压力反射调节仍然存在，直到它被具有相对心动过缓和动脉阻力血管舒张的相反降压反射抵消。与血管迷走神经反应相关的血管舒张的性质仍未确定。
