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迷走神经刺激后心动过速的实验分析。

An experimental analysis of the tachycardia that follows vagal stimulation.

作者信息

Burke G H, Calaresu F R

出版信息

J Physiol. 1972 Oct;226(2):491-510. doi: 10.1113/jphysiol.1972.sp009995.

Abstract
  1. Postvagal tachycardia, the transient increase in heart rate that follows the sinus bradycardia elicited by vagal stimulation, was investigated in thirty chloralosed cats. Maximum postvagal tachycardia was elicited by stimulation at frequencies of 20-60 Hz with train durations of 30-90 sec. A positive correlation was demonstrated between the magnitudes of postvagal tachycardia and of the preceding sinus bradycardia.2. Postvagal tachycardia was not affected by either spinal transection at C7 or by administration of propranolol (1.5 mg/kg I.V.), but was abolished by the administration of atropine (2.0 mg/kg I.V.).3. Postvagal tachycardia was observed to follow the vagal bradycardia induced reflexly either by administration of phenyldiguanide (100-300 mug I.V.) or by stimulation of the aortic depressor nerve.4. In the isolated atria-vagus preparations from six rabbits a positive correlation was demonstrated between the magnitude of postvagal tachycardia and of the preceding bradycardia elicited by vagal stimulation.5. Continuous intracellular recordings were obtained from four sinuatrial node pace-maker cells in the isolated atria-vagus preparation of the rabbit before, during and after vagal stimulation. During postvagal tachycardia the slope of the diastolic prepotential, the maximum diastolic potential, threshold potential and the overshoot were found to be increased; these changes are different from those found in pace-maker cells during adrenergic activation.6. These findings demonstrate that postvagal tachycardia is not mediated by sympathetic adrenergic mechanisms, but suggest that it is dependent upon the preceding vagal bradycardia and may be related to an increase in net sodium influx into pace-maker cells initiated by the hyperpolarization of the pace-maker cell membrane during and immediately after vagal stimulation.
摘要
  1. 迷走神经刺激引发窦性心动过缓后出现的短暂心率增加即迷走神经后心动过速,在30只水合氯醛麻醉的猫身上进行了研究。以20 - 60赫兹的频率、30 - 90秒的串刺激可诱发最大迷走神经后心动过速。迷走神经后心动过速的幅度与先前窦性心动过缓的幅度之间呈正相关。

  2. 迷走神经后心动过速不受C7水平脊髓横断或静脉注射普萘洛尔(1.5毫克/千克)的影响,但静脉注射阿托品(2.0毫克/千克)可消除该现象。

  3. 观察到静脉注射苯二胍(100 - 300微克)或刺激主动脉减压神经反射性诱发迷走性心动过缓后会出现迷走神经后心动过速。

  4. 在6只兔子的离体心房 - 迷走神经标本中,迷走神经后心动过速的幅度与迷走神经刺激引发的先前心动过缓的幅度之间呈正相关。

  5. 在兔子离体心房 - 迷走神经标本中,对4个窦房结起搏细胞在迷走神经刺激前、刺激期间和刺激后进行了连续的细胞内记录。在迷走神经后心动过速期间,舒张期预电位斜率、最大舒张电位、阈电位和超射均增加;这些变化与肾上腺素能激活期间起搏细胞中的变化不同。

  6. 这些发现表明,迷走神经后心动过速不是由交感肾上腺素能机制介导的,但提示其依赖于先前的迷走性心动过缓,并且可能与迷走神经刺激期间及之后起搏细胞膜超极化引发的起搏细胞净钠内流增加有关。

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A reversed action of the vagus on the mammalian heart.迷走神经对哺乳动物心脏的反向作用。
J Physiol. 1910 Oct 11;41(1-2):1-18. doi: 10.1113/jphysiol.1910.sp001391.
3
Circulatory and respiratory reflexes caused by aromatic guanidines.芳香胍类引起的循环和呼吸反射。
Br J Pharmacol Chemother. 1950 Mar;5(1):65-76. doi: 10.1111/j.1476-5381.1950.tb00578.x.

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