THE BEZOLD-JARISCH REFLEX REVISITED - CLINICAL IMPLICATIONS OF INHIBITORY REFLEXES ORIGINATING IN THE HEART
THE BEZOLD-JARISCH REFLEX REVISITED - CLINICAL IMPLICATIONS OF INHIBITORY REFLEXES ORIGINATING IN THE HEART
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DOI：
10.1016/s0735-1097(83)80014-x
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发表时间：
1983-01-01
影响因子：
24
通讯作者：
MARK, AL
中科院分区：
文献类型：
--
作者：
MARK, AL
抑制反射起源于心脏的概念由冯·贝佐尔德 (von Bezold) 于 1867 年提出，后来由贾里什 (Jarisch) 复兴。 Bezold-Jarisch 反射起源于具有非髓鞘迷走神经传入途径的心脏感觉受体。左心室，特别是下后壁，是这些感觉感受器的主要位置。通过拉伸、化学物质或药物刺激这些抑制性心脏受体会增加副交感神经活动并抑制交感神经活动。这些作用可促进反射性心动过缓、血管舒张和低血压（Bezold-Jarisch 反射），还可调节肾素释放和加压素分泌。相反，这些抑制性感觉受体活性的降低会反射性地增加交感神经活性、血管阻力、血浆肾素活性和加压素。长期以来，这些抑制性心脏感觉受体的反射一直被认为是药理学的好奇心，但现在已经清楚，起源于这些抑制性心脏感觉受体的反射对于许多心血管疾病的病理生理学很重要。本文综述了抑制性心脏感觉受体在几种临床状态中的作用，包括 1) 心动过缓、低血压和胃肠道疾病伴下后壁心肌缺血和梗死，2) 冠状动脉造影期间心动过缓和低血压，3) 主动脉瓣狭窄中的劳力性晕厥，4) 血管迷走性晕厥，5) 神经体液性晕厥 慢性心力衰竭的兴奋，6）洋地黄的治疗作用。
The concept of depressor reflexes originating in the heart was introduced by von Bezold in 1867 and was later revived by Jarisch. The Bezold-Jarisch reflex originates in cardiac sensory receptors with nonmyelinated vagal afferent pathways. The left ventricle, particularly the inferoposterior wall, is a principal location for these sensory receptors. Stimulation of these inhibitory cardiac receptors by stretch, chemical substances or drugs increases parasympathetic activity and inhibits sympathetic activity. These effects promote reflex bradycardia, vasodilation and hypotension (Bezold-Jarisch reflex) and also modulate renin release and vasopressin secretion. Conversely, decreases in the activity of these inhibitory sensory receptors reflexly increase sympathetic activity, vascular resistance, plasma renin activity and vasopressin.Long regarded as pharmacologic curiosities, it is now clear that reflexes originating in these inhibitory cardiac sensory receptors are important to the pathophysiology of many cardiovascular disorders. This paper reviews the role of inhibitory cardiac sensory receptors in several clinical states including 1) bradycardia, hypotension and gastrointestinal disorders with inferoposterior myocardial ischemia and infarction, 2) bradycardia and hypotension during coronary arteriography, 3) exertional syncope in aortic stenosis, 4) vasovagal syncope, 5) neurohumoral excitation in chronic heart failure, and 6) the therapeutic effects of digitalis.