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迷走神经诱导的阻滞和延迟传导作为青蛙心房中环行运动性心动过速的一种机制。

Vagally induced block and delayed conduction as a mechanism for circus movement tachycardia in frog atria.

作者信息

Rosenshtraukh L V, Zaitsev A V, Fast V G, Pertsov A M, Krinsky V I

机构信息

Institute of Experimental Cardiology, Cardiology Research Center, Moscow, USSR.

出版信息

Circ Res. 1989 Feb;64(2):213-26. doi: 10.1161/01.res.64.2.213.

DOI:10.1161/01.res.64.2.213
PMID:2783563
Abstract

Episodes of tachycardia induced by strong vagal stimulation in spontaneously beating isolated atria of frog (Rana temporaria) were studied with multielectrode mapping technique. These episodes were inducible in 19 of 39 preparations. The arrhythmia started several seconds after cessation of vagal stimulation strong enough to cause sinus arrest, without electrical stimulation of the myocardium. The arrhythmia consisted of two to 20 beats (6 +/- 4, mean +/- SD, n = 42) with a cycle length of 100-500 msec. Recording from 32 sites with spatial resolution of 1-2 mm showed that the arrhythmia was due to intra-atrial circus movement. The estimated perimeter of the reentrant circuit ranged from 6 to 20 mm. In circuits of the minimal size, the average conduction velocity along the circuit was as low as 2-3 cm/sec. Paroxysms of the tachycardia were always preceded by vagally induced nonuniform depression of conduction, with some areas of atria being completely blocked. As the vagal influence decreased, the blocked areas recovered in an inhomogeneous manner, their unblocking being significantly (p less than 0.05) delayed after inhibition of tissue cholinesterase by proserine. The reentrant tachycardia was initiated when a sinus impulse arrived during certain phase of the unblocking. Unlike the well-known mechanism of reentrant excitation, which is based on inhomogeneous refractoriness and critically timed extrabeat(s), the circus movement in our model depended on vagally induced conduction block and could be launched by a single sinus impulse.

摘要

采用多电极标测技术,对青蛙(林蛙)自主搏动的离体心房中由强烈迷走神经刺激诱发的心动过速发作进行了研究。在39份标本中有19份可诱发这些发作。心律失常在足以导致窦性停搏的迷走神经刺激停止后数秒开始,无需对心肌进行电刺激。心律失常由2至20次搏动组成(6±4,平均值±标准差,n = 42),心动周期为100 - 500毫秒。以1 - 2毫米的空间分辨率从32个位点进行记录表明,心律失常是由于心房内折返运动所致。折返环的估计周长为6至20毫米。在最小尺寸的环路中,沿环路的平均传导速度低至2 - 3厘米/秒。心动过速发作之前总是先出现迷走神经诱发的传导不均匀性抑制,心房的某些区域完全阻滞。随着迷走神经影响减弱,阻滞区域以不均匀的方式恢复,在毒扁豆碱抑制组织胆碱酯酶后,其解除阻滞明显延迟(p < 0.05)。当窦性冲动在解除阻滞的特定阶段到达时,折返性心动过速就会开始。与基于不均匀不应期和关键定时早搏的众所周知的折返激动机制不同,我们模型中的折返运动依赖于迷走神经诱发的传导阻滞,并且可以由单个窦性冲动引发。

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Vagally induced block and delayed conduction as a mechanism for circus movement tachycardia in frog atria.迷走神经诱导的阻滞和延迟传导作为青蛙心房中环行运动性心动过速的一种机制。
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