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肾性高血压大鼠肥厚心肌中的后电位和触发活动。

Afterpotentials and triggered activity in hypertrophied myocardium from rats with renal hypertension.

作者信息

Aronson R S

出版信息

Circ Res. 1981 May;48(5):720-7. doi: 10.1161/01.res.48.5.720.

Abstract

We have found that afterpotentials can be induced selectively in hypertrophied myocardium from rats with renal hypertension. Three kinds of afterpotentials were recorded by standard microelectrode techniques: early afterdepolarizations, delayed afterdepolarizations, and early afterdepolarizations. The first two kinds of afterpotentials could give rise to triggered spontaneous activity, whereas the last kind did not. Delayed afterdepolarizations were induced in hypertrophied fibers exposed to Tyrode's solution containing high extracellular calcium ([Ca2+]o = 7.2-12 mM) and early afterdepolarizations occurred in hypertrophied fibers exposed to Tyrode's solution containing tetraethylammonium (TEA = 10-30 mM). Neither of these treatments produced afterpotentials in normal myocardium. We found that delayed afterdepolarizations became larger when the stimulation frequency, number of preceding driven beats, or [Ca2+]o was increased. The coupling interval from the upstroke of the last driven action potential to the peak of the delayed afterdepolarization decreased when the stimulation frequency or number of preceding driven beats increased. Hypertrophied fibers treated with high [Ca2+]o that gave rise to triggered activity showed a characteristic relationship between delayed afterpotential magnitude and drive cycle length. In hypertrophied muscles treated with TEA, triggered activity developed from an early afterdepolarizations but terminated with a delayed afterdepolarization. The occurrence of afterpotentials in hypertrophied, but not in normal myocardium, appears to reflect the development of an important electrophysiological alteration that may predispose hypertrophied fibers to develop arrhythmias.

摘要

我们发现,在肾性高血压大鼠的肥厚心肌中可选择性地诱发后电位。采用标准微电极技术记录到了三种后电位:早期后去极化、延迟后去极化和早期后去极化。前两种后电位可引发触发自发性活动,而最后一种则不能。在暴露于含高细胞外钙([Ca2+]o = 7.2 - 12 mM)的台氏液中的肥厚纤维中诱发了延迟后去极化,在暴露于含四乙铵(TEA = 10 - 30 mM)的台氏液中的肥厚纤维中出现了早期后去极化。这两种处理在正常心肌中均未产生后电位。我们发现,当刺激频率、前驱动搏动次数或[Ca2+]o增加时,延迟后去极化会变大。当刺激频率或前驱动搏动次数增加时,从最后一个驱动动作电位的上升支到延迟后去极化峰值的耦合间期缩短。用高[Ca2+]o处理并引发触发活动的肥厚纤维显示出延迟后电位幅度与驱动周期长度之间的特征性关系。在用TEA处理的肥厚肌肉中,触发活动从早期后去极化发展而来,但以延迟后去极化结束。后电位出现在肥厚心肌而非正常心肌中,这似乎反映了一种重要的电生理改变的发展,这种改变可能使肥厚纤维易发生心律失常。

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