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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Myocardial Ca2+ handling and cell-to-cell coupling, key factors in prevention of sudden cardiac death.
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Myocardial Ca2+ handling and cell-to-cell coupling, key factors in prevention of sudden cardiac death.

机译：心肌Ca2 +的处理和细胞间的偶联是预防心源性猝死的关键因素。

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Using whole-heart preparations, we tested our hypothesis that Ca(2+) handling is closely related to cell-to-cell coupling at the gap junctions and that both are critical for the development and particularly the termination of ventricular fibrillation (VF) and hence the prevention of sudden arrhythmic death. Intracellular free calcium concentration ([Ca(2+)](i)), ECG, and left ventricular pressure were continuously monitored in isolated guinea pig hearts before and during development of low K(+)-induced sustained VF and during its conversion into sinus rhythm facilitated by stobadine. We also examined myocardial ultrastructure to detect cell-to-cell coupling alterations. We demonstrated that VF occurrence was preceded by a 55.9% +/- 6.2% increase in diastolic [Ca(2+)](i), which was associated with subcellular alterations indicating Ca(2+) overload of the cardiomyocytes and disorders in coupling among the cells. Moreover, VF itself further increased [Ca(2+)](i) by 58.2% +/- 3.4% and deteriorated subcellular and cell-to-cell coupling abnormalities that were heterogeneously distributed throughout the myocardium. In contrast, termination of VF and its conversion into sinus rhythm was marked by restoration of basal [Ca(2+)](i), resulting in recovery of intercellular coupling linked with synchronous contraction. Furthermore, we have shown that hearts exhibiting lower SERCA2a (sarcoplasmic reticulum Ca(2+)-ATPase) activity and abnormal intercellular coupling (as in older guinea pigs) are more prone to develop Ca(2+) overload associated with cell-to-cell uncoupling than hearts with higher SERCA2a activity (as in young guinea pigs). Consequently, young animals are better able to terminate VF spontaneously. These findings indicate the crucial role of Ca(2+) handling in relation to cell-to-cell coupling in both the occurrence and termination of malignant arrhythmia.
机译：使用全心准备，我们测试了我们的假设，即Ca（2+）处理与间隙连接处的细胞间耦合密切相关，并且两者都对发育尤其是心室纤颤（VF）的终止和因此，预防心律失常性猝死。在低K（+）诱导的持续性VF形成之前和过程中以及转化为VF的过程中，连续监测离体豚鼠心脏的细胞内游离钙浓度（[Ca（2 +）]（i）），ECG和左心室压力stobadine促进窦性心律。我们还检查了心肌的超微结构，以检测细胞间的耦合变化。我们证明VF发生之前舒张性[Ca（2 +）]（i）增加55.9％+/- 6.2％，这与亚细胞改变有关，表明心肌细胞Ca（2+）超负荷和耦合障碍在细胞之间。此外，VF本身使[Ca（2 +）]（i）进一步增加了58.2％+/- 3.4％，并恶化了分布在整个心肌中的亚细胞和细胞间偶联异常。相反，VF的终止及其向窦性心律的转变以基底[Ca（2 +）]（i）的恢复为标志，导致恢复了与同步收缩相关的细胞间偶联。此外，我们已经表明，表现出较低的SERCA2a（肌浆网Ca（2 +）-ATPase）活性和异常的细胞间偶联（如在老年的豚鼠中）的心脏更容易出现与细胞间相关的Ca（2+）超负荷。细胞的解偶联作用比具有更高SERCA2a活性的心脏的解偶联作用（如年轻的豚鼠）。因此，幼小动物能够更好地自发终止VF。这些发现表明，在恶性心律不齐的发生和终止中，Ca（2+）处理与细胞间偶联相关的关键作用。

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