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犬压力超负荷所致衰竭心脏的细胞内、外电解质及肌膜ATP酶

Intra- and extracellular electrolytes and sarcolemmal ATPase in the failing heart due to pressure overload in dogs.

作者信息

Prasad K, Khatter J C, Bharadwaj B

出版信息

Cardiovasc Res. 1979 Feb;13(2):95-104. doi: 10.1093/cvr/13.2.95.

Abstract

An investigation of changes in the Mg2+ -dependent, Na+ -K+ -stimulated sarcolemmal ATPase and of intracellular electrolytes in the left failing heart due to pressure overload (aortic banding) was carried out in dogs. There was no change in the sarcolemmal Mg2+ -ATPase of the left or right ventricle for the whole duration (3 to 9 months) of left ventricular pressure overload. In the early phase (3 months) of aortic banding, when there was no haemodynamic evidence of left ventricular failure, there was also no significant change in the sarcolemmal Na+ -K+ -ATPase, extracellular space, or intra- and extracellular electrolytes. However, during 6 to 9 months of aortic binding when there was haemodynamic evidence of left ventricular failure (increased end-diastolic pressure, decreased cardiac index and (dP/dt)/IIP, enlarged heart), there was also a marked increase in the left ventricular sarcolemmal Na+ -K+ -ATPase and intracellular K+; and a decrease in the intracellular Na+ and Ca2+. The extracellular space in the left ventricle also increased significantly. Unlike the left ventricle, the right ventricle did not show any evidence of failure, not did it show any change in the sarcolemmal Na+ -K+ -ATPase and intracellular electrolytes during any period of aortic banding. These results suggest that the decrease in the myocardial contractility in failing heart due to pressure overload might be associated with a decrease in the intracellular Ca2+ as a result of an increase in the sarcolemmal Na+ -K+ -ATPase.

摘要

在犬类动物身上进行了一项研究,旨在探究因压力超负荷(主动脉缩窄)导致左心衰竭时,镁离子依赖性、钠钾离子刺激的肌膜ATP酶以及细胞内电解质的变化情况。在左心室压力超负荷的整个持续期间(3至9个月),左心室或右心室的肌膜镁离子ATP酶均未发生变化。在主动脉缩窄的早期阶段(3个月),当尚无左心室衰竭的血流动力学证据时,肌膜钠钾离子ATP酶、细胞外间隙以及细胞内和细胞外电解质也均无显著变化。然而,在主动脉缩窄6至9个月期间,当出现左心室衰竭的血流动力学证据(舒张末期压力升高、心脏指数降低以及(dP/dt)/IIP降低、心脏增大)时,左心室肌膜钠钾离子ATP酶和细胞内钾离子也显著增加;细胞内钠离子和钙离子则减少。左心室的细胞外间隙也显著增加。与左心室不同,右心室未显示任何衰竭迹象,在主动脉缩窄的任何时期,其肌膜钠钾离子ATP酶和细胞内电解质也均未发生变化。这些结果表明,压力超负荷导致的衰竭心脏心肌收缩力下降可能与肌膜钠钾离子ATP酶增加致使细胞内钙离子减少有关。

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