Functional properties of failing human ventricular myocytes

被引：37

作者：

Houser, SR ^{[1
]}

Piacentino, V ^{[1
]}

Mattiello, J ^{[1
]}

Weisser, J ^{[1
]}

Gaughan, JP ^{[1
]}

机构：

[1] Temple Univ, Sch Med, Cardiovasc Res Grp, Mol & Cellular Cardiol Labs, Philadelphia, PA 19140 USA

来源：

TRENDS IN CARDIOVASCULAR MEDICINE | 2000年 / 10卷 / 03期

关键词：

D O I：

10.1016/S1050-1738(00)00057-8

中图分类号：

R5 [内科学];

学科分类号：

1002 ; 100201 ;

摘要：

Reduced peak systolic Ca2+ and slow decay of the Ca2+ transient are common features of the end-stage failing human ventricular myocyte and ave thought to underlie abnormal ventricular contractility in congestive heart failure (CHF), Individual changes in the expression or activity of Ca2+ transport proteins of the sarcoplasmic reticulum (SR Ca2+ ATPase, SERCa) or the sarcolemmal (sodium-calcium exchanger, NCX) have not always been observed in CHF and cannot per se consistently explain these Ca2+ transient defects, We review recent data that suggests that the normal balance of transport activities of SERCa and NCX is deranged in failing human myocytes. We hypothesize that an increase in the NCX/SERCa transport capacity in failing myocytes can explain the abnormal Ca2+ homeostasis of the failing human ventricular myocyte. (C) 2001, Elsevier Science Inc.

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收藏

页码：101 / 107

页数：7

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