钾对大鼠心脏心律失常发生的允许作用。

Permissive action of potassium on arrhythmogenesis in the rat heart.

作者信息

Lubbe W F, Holland R K, Gilchrist A I, Pybus J

出版信息

J Mol Cell Cardiol. 1986 Oct;18 Suppl 4:37-41. doi: 10.1016/s0022-2828(86)80024-4.

Abstract

The isolated perfused rat heart was used to assess the influence of extracellular potassium ([K+]0) on vulnerability of the heart to ventricular fibrillation (VF). The VF threshold is reduced when [K+]0 is lowered from 5.9 to 2.0 and 3.0 mmol/l. The vulnerable period is not only widened but VF can be obtained by stimuli on the R wave. The opposite effects are encountered when [K+]0 is increased to 9.0 mmol/l. These alterations in vulnerability to VF are accompanied by an increased incidence of tachyarrhythmias and spontaneous VF during coronary artery ligation and following reperfusion on reduction of [K+]0, with elimination of these arrhythmias on increasing [K+]0 to 9.0 mmol/l. The cellular biochemical responses that accompanied the altered electrical behaviour on alterations of [K+]0 involved the tissue levels of cyclic AMP in both non-ischaemic and ischaemic myocardium and tissue levels of Ca2+ whereas tissue levels of high energy phosphates, adenosine, inosine, hypoxanthine, lactate, Na+, K+ and Mg2+ did not discriminate between hearts vulnerable and hearts resistant to VF. In this model the extracellular K+ level is a determinant of vulnerability to ventricular fibrillation while ischaemic tissue levels of Ca2+ provide the best correlation with alterations in vulnerability.

摘要

采用离体灌流大鼠心脏来评估细胞外钾离子浓度（[K⁺]₀）对心脏心室颤动（VF）易损性的影响。当[K⁺]₀从5.9 mmol/L降至2.0 mmol/L和3.0 mmol/L时，VF阈值降低。易损期不仅变宽，而且在R波上施加刺激可诱发VF。当[K⁺]₀增加到9.0 mmol/L时，会出现相反的效果。在冠状动脉结扎期间及再灌注后，随着[K⁺]₀降低，VF易损性的这些改变伴随着快速性心律失常和自发性VF发生率的增加，而将[K⁺]₀增加到9.0 mmol/L可消除这些心律失常。随着[K⁺]₀改变，电行为发生改变，伴随的细胞生化反应涉及非缺血和缺血心肌中环磷酸腺苷（cAMP）的组织水平以及Ca²⁺的组织水平，而高能磷酸盐、腺苷、肌苷、次黄嘌呤、乳酸、Na⁺、K⁺和Mg²⁺的组织水平在易发生VF的心脏和对VF有抵抗力的心脏之间并无差异。在该模型中，细胞外钾离子水平是心室颤动易损性的一个决定因素，而缺血组织中的Ca²⁺水平与易损性改变的相关性最佳。