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心脏节律的自主神经控制:自主神经失衡在心律失常发生中的作用。

Autonomic neural control of cardiac rhythm: the role of autonomic imbalance in the genesis of cardiac dysrhythmia.

作者信息

Randall W C, Euler D E, Jacobs H K, Wehrmacher W, Kaye M P, Hageman G R

出版信息

Cardiology. 1976;61(1):20-36. doi: 10.1159/000169745.

DOI:10.1159/000169745
PMID:975122
Abstract

Cardiac dysrhythmias result from abnormalities in rate, regularity, or sequence of cardiac activation, and because of direct actions of the autonomic nervous system upon each of these properties, imbalance in this system may play an important role in the genesis of cardiac dysrhythmia. A canine model has been developed in which the extrinsic innervation of the heart is ablated with the exception of the ventrolateral cardiac nerve. This nerve is distributed primarily to the inferior atrial, AV junctional, and ventricular tissues. Following recovery from surgery, the animal is placed on a treadmill and required to perform strenuous exercise. In all of six animals which sustained repeated exercise testing over periods of 4-12 months, dysrhythmias of varying complexities were elicited. None appeared in parallel experiments conducted in control or sham-operated animals. The dysrhythmias consisted of supraventricular, AV junctional, or ventricular tachycardias with occasional premature atrial or ventricular systoles. The dysrhythmias were not influenced by atropine but were generally controlled by propranolol.

摘要

心律失常是由心脏激动的速率、节律或顺序异常引起的,由于自主神经系统对这些特性中的每一个都有直接作用,该系统的失衡可能在心律失常的发生中起重要作用。已经建立了一种犬类模型,其中除了心脏腹外侧神经外,心脏的外在神经支配被切除。这条神经主要分布在下心房、房室交界区和心室组织。手术后恢复后,将动物置于跑步机上并要求其进行剧烈运动。在所有六只经过4至12个月反复运动测试的动物中,均引发了不同复杂性的心律失常。在对照或假手术动物进行的平行实验中未出现心律失常。心律失常包括室上性、房室交界区性或室性心动过速,偶尔伴有房性或室性早搏。这些心律失常不受阿托品影响,但通常可被普萘洛尔控制。

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Ultrastructural preservation of human atrial intrinsic innervation after the cold ischemic anoxic asystole during cardiac surgery.心脏手术期间冷缺血性缺氧心搏停止后人心房固有神经支配的超微结构保存
Experientia. 1980 Oct 15;36(10):1189-91. doi: 10.1007/BF01976120.
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Role of sympathetic nervous system in non-ischaemic ventricular arrhythmias.
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Br Heart J. 1982 Feb;47(2):137-47. doi: 10.1136/hrt.47.2.137.