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[刺激迷走神经后房性快速心律失常的发生机制]

[The mechanism of the development of atrial tachyarrhythmia after stimulation of the vagus nerve].

作者信息

Rozenshtraukh L V, Zaĭtsev A V, Pertsov A M, Fast V G, Krinskiĭ V I

出版信息

Kardiologiia. 1988 Feb;28(2):79-84.

PMID:3259649
Abstract

Multielectrode mapping of stimulus propagation was used to investigate arrhythmias, developing in atrial preparations of frogs after vagal stimulation. Vagal stimulation produced attacks of tachycardia (one to several dozens extra-excitations) in 10 of 16 specimens. In such cases, mapping demonstrated re-entry of the excitation wave that appeared where the front of the next excitation wave from the sinus went along the border of temporarily-unexcitable area during the recovery of excitability in vagus-inhibited atrial areas. The emergence of re-entry was possible, because the excitation wave length (lambda), was shortened owing to reduced refraction and speed of conduction under vagal effect. After myocardial tissue got rid of vagal influence, lambda increased, after which re-entry was no longer possible, and arrhythmia discontinued.

摘要

采用多电极刺激传播映射技术研究迷走神经刺激后青蛙心房标本中发生的心律失常。在16个标本中,有10个在迷走神经刺激后出现心动过速发作(一到几十次额外兴奋)。在这种情况下,映射显示兴奋波的折返,其出现在迷走神经抑制的心房区域兴奋性恢复期间,来自窦房结的下一个兴奋波前沿沿着暂时不可兴奋区域的边界行进的地方。折返的出现是可能的,因为在迷走神经作用下,由于折射降低和传导速度减慢,兴奋波长(λ)缩短。心肌组织摆脱迷走神经影响后,λ增加,此后折返不再可能,心律失常停止。

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