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心动过速性心肌病早期恢复后的左心室及心肌细胞结构与功能

LV and myocyte structure and function after early recovery from tachycardia-induced cardiomyopathy.

作者信息

Spinale F G, Holzgrefe H H, Mukherjee R, Arthur S R, Child M J, Powell J R, Koster W H

机构信息

Division of Cardiothoracic Surgery, Medical University of South Carolina, Charleston 29425.

出版信息

Am J Physiol. 1995 Feb;268(2 Pt 2):H836-47. doi: 10.1152/ajpheart.1995.268.2.H836.

DOI:10.1152/ajpheart.1995.268.2.H836
PMID:7864211
Abstract

Left ventricular (LV) function and mass were measured in six conscious dogs at weekly intervals during the progression of tachycardia-induced dilated cardiomyopathy (DCM) and during a 1-mo recovery period from DCM (post-DCM). LV end-diastolic volume and LV wall stress increased and LV ejection fraction decreased with each week of pacing. Despite the increased LV wall stress, LV mass did not change during the progression of tachycardia DCM. One week post-DCM resulted in an improved LV ejection fraction and normalization of neurohormonal profiles. However, 1 wk post-DCM was accompanied by a 26% increase in LV mass and persistent LV chamber dilation. Isolated myocyte function was examined and compared with that in six normal control dogs. Myocyte percent and myocyte velocity of shortening were 19 and 32% lower, respectively, in the post-DCM group compared with controls. Thus termination of the tachycardia subsequent to the development of DCM resulted in persistent LV chamber dilation and abnormalities in myocyte contractile function. The improved LV pump function with early recovery from tachycardia-induced DCM was mediated by LV hypertrophy and a subsequent reduction in LV wall stress rather than a normalization of LV geometry and myocyte contractile function.

摘要

在心动过速诱发的扩张型心肌病(DCM)进展过程中以及从DCM恢复的1个月期间(DCM后),每周对6只清醒犬的左心室(LV)功能和质量进行测量。随着起搏周数的增加,左心室舒张末期容积和左心室壁应力增加,左心室射血分数降低。尽管左心室壁应力增加,但在心动过速性DCM进展过程中左心室质量并未改变。DCM后1周,左心室射血分数有所改善,神经激素水平恢复正常。然而,DCM后1周,左心室质量增加了26%,左心室腔持续扩张。对分离的心肌细胞功能进行了检测,并与6只正常对照犬的心肌细胞功能进行了比较。与对照组相比,DCM后组的心肌细胞缩短百分比和心肌细胞缩短速度分别降低了19%和32%。因此,在DCM发展后终止心动过速会导致左心室腔持续扩张和心肌细胞收缩功能异常。心动过速诱发的DCM早期恢复时左心室泵功能的改善是由左心室肥厚和随后左心室壁应力的降低介导的,而不是左心室几何形状和心肌细胞收缩功能的正常化。

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