微电泳法观察去甲肾上腺素对兔心房起搏器不同细胞的影响。

Archivio di scienze biologiche Pub Date : 1978-01-01
G L Avanzino, R Ermirio
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引用次数: 0

摘要

用微电泳法将去甲肾上腺素应用于兔心脏心房起搏器区域的一小部分,以便将这种化学递质与起搏器区域其他部分的递质分开研究其局部作用。在第一组细胞中,它们的动作电位和位置将它们同化为真正的起搏器细胞,去甲肾上腺素导致周期长度的减少和舒张期缓慢去极化的陡度的增加。在第二组与潜伏起搏器细胞相似的细胞中,去甲肾上腺素没有引起周期长度的变化,其显著作用是增加了舒张期缓慢去极化的陡峭程度,随后转变为阈下振荡。第三种类型的细胞表现出介于前两组之间的中间特征。这些结果表明:a)去甲肾上腺素对心房起搏器的变时作用似乎是由于舒张期缓慢去极化的陡峭程度的改变,在某些情况下,可以假设阈下振荡的形状;在我们的准备过程中,对其他参数的影响似乎不是不那么稳定就是不那么显著;B)对各种细胞产生的不同作用似乎是对去甲肾上腺素的不同程度的敏感性以及或多或少地过早激活对抗去甲肾上腺素作用的机制的结果。这些结果是在最近提出的自发心房起搏模型的基础上进行讨论的。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The effects of noradrenaline, applied by microelectrophoresis on different cells of the rabbit's atrial pacemaker.

Noradrenaline has been applied by microelectrophoresis to a small portion of the atrial pacemaker area in the rabbit's heart in order to study the local effects of this chemical transmitter separately from the ones deriving from other parts of the pacemaker area. In a first group of cells, whose action potential and location assimilate them to true pacemaker cells, noradrenaline caused a reduction in cycle length and an increase in the steepness of slow diastolic depolarization. In a second group of cells similar to latent pacemaker cells, noradrenaline caused no change in cycle length, the outstanding effect being an increase in the steepness of the slow diastolic depolarization which afterwards changed into a subthreshold oscillation. A third type of cells showed intermediate characteristics between the two previous groups. These results suggest that: a) the chronotropic effect of noradrenaline on the heart atrial pacemaker seems to be due to changes in the steepness of slow diastolic depolarization which can assume, in some instances, the shape of subthreshold oscillations; the effects on the other parameters in our preparation seem to be either less constant or less significant; b) the different effects which are obtained on various kinds of cells seem to be the result of a different degree of sensitivity to noradrenaline and to the more or less premature activation of mechanisms antagonizing the action of noradrenaline. The results are discussed on the basis of a model of spontaneous atrial pacemaking which has been recently proposed.

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