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铯、细胞内钠活性与心脏浦肯野纤维起搏电位之间的相互关系。

The interrelationship of cesium, intracellular sodium activity, and pacemaker potential in cardiac Purkinje fibers.

作者信息

Iacono G, Vassalle M

机构信息

Department of Physiology, State University of New York, Brooklyn 11203.

出版信息

Can J Physiol Pharmacol. 1990 Sep;68(9):1236-46. doi: 10.1139/y90-186.

Abstract

The actions of cesium (Cs) on intracellular sodium activity (aiNa), membrane potentials, and force were studied in sheep cardiac Purkinje and myocardial fibers superfused in vitro. In Purkinje fibers, Cs (2 mM) decreased diastolic depolarization, aiNa (-6.7%, p less than 0.005), and force (-28.0%, p less than 0.01). The effects of 4 and 8 mM Cs were more pronounced. In quiescent fibers, Cs (2-4 mM) also decreased aiNa (-17.3%, p less than 0.005) and induced an initial hyperpolarization (+5.6 +/- 1.3%, p less than 0.005) followed by a return toward control. Diastolic depolarization was almost abolished by driving the fibers at 180/min (diastole was very short) but still Cs decreased aiNa (-15.4%). Tetrodotoxin decreased aiNa (-16.2%, p less than 0.025) and reduced the Cs-induced fall in aiNa (-2.2%, p less than 0.05). In zero [K]o, Cs decreased aiNa and caused repolarization. In 0.1 mM strophanthidin, Cs did not decrease aiNa any longer and affected the membrane potential little. In quiescent myocardial fibers, Cs (4 mM) decreased aiNa (-12.6%, p less than 0.05) and transiently hyperpolarized (+2.1%). Rubidium (2 mM) decreased aiNa and resting potential in Purkinje fibers and in myocardial fibers and also decreased diastolic depolarization in Purkinje fibers. Thus, cesium and rubidium decrease aiNa and modify the membrane potential but not through a block of the inward pacemaker current If.

摘要

在体外灌流的绵羊心脏浦肯野纤维和心肌纤维中,研究了铯(Cs)对细胞内钠活性(aiNa)、膜电位和张力的作用。在浦肯野纤维中,2 mM的Cs可降低舒张期去极化、aiNa(-6.7%,p<0.005)和张力(-28.0%,p<0.01)。4 mM和8 mM Cs的作用更明显。在静息纤维中,2-4 mM的Cs也可降低aiNa(-17.3%,p<0.005),并引起初始超极化(+5.6±1.3%,p<0.005),随后恢复到对照水平。以180次/分钟驱动纤维(舒张期非常短)时,舒张期去极化几乎被消除,但Cs仍可降低aiNa(-15.4%)。河豚毒素可降低aiNa(-16.2%,p<0.025),并减少Cs诱导的aiNa下降(-2.2%,p<0.05)。在零[K]o中,Cs可降低aiNa并导致复极化。在0.1 mM毒毛花苷中,Cs不再降低aiNa,对膜电位影响很小。在静息心肌纤维中,4 mM的Cs可降低aiNa(-12.6%,p<0.05)并短暂超极化(+2.1%)。2 mM的铷可降低浦肯野纤维和心肌纤维中的aiNa和静息电位,也可降低浦肯野纤维中的舒张期去极化。因此,铯和铷可降低aiNa并改变膜电位,但不是通过阻断内向起搏电流If。

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