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镁在心脏浦肯野纤维中的抗心律失常机制

On the antiarrhythmic mechanisms of magnesium in cardiac Purkinje fibers.

作者信息

Aceto E, Vassalle M

机构信息

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

出版信息

Magnes Trace Elem. 1991;10(5-6):355-63.

PMID:1669019
Abstract

The antiarrhythmic actions of high [Mg]o (8 mM) were studied in sheep cardiac Purkinje fibers. At 0.1 microM, strophanthidin inhibits the Na-K pump (intracellular sodium activity aiNa and force increase) and increasing Mg shortens the action potential, decreases force and increases aiNa, as in control. At 1 microM, strophanthidin increases aiNa and force, induces oscillatory potentials (Vos) and arrhythmias: increasing Mg reduces Vos and abolishes arrhythmias but increases aiNa further. High Mg also slows or stops spontaneous activity induced by norepinephrine by a positive shift of the threshold, and decreases Vos in high [Ca]o. Thus, antiarrhythmic mechanisms of high [Mg]o include a shift in threshold potential and a decrease in Vos but not a removal of Na pump inhibition.

摘要

在绵羊心脏浦肯野纤维中研究了高细胞外镁浓度(8 mM)的抗心律失常作用。在0.1微摩尔时,毒毛花苷抑制钠钾泵(细胞内钠活性aiNa和张力增加),增加镁会缩短动作电位、降低张力并增加aiNa,与对照组情况相同。在1微摩尔时,毒毛花苷增加aiNa和张力,诱发振荡电位(Vos)和心律失常:增加镁可减少Vos并消除心律失常,但会进一步增加aiNa。高镁还通过阈值的正向偏移减缓或停止去甲肾上腺素诱导的自发活动,并在高细胞外钙浓度时降低Vos。因此,高细胞外镁浓度的抗心律失常机制包括阈值电位的偏移和Vos的降低,但不包括解除对钠泵的抑制。

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