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[心力衰竭中的分子病理生物学]

[Molecular pathobiology in heart failure].

作者信息

Reis-Santos K, André C, Fernandes S V, Barros F, Pinto S, Centeno A M, Costa P, Serra D, Campos P M, Godinho F

机构信息

Faculdade de Medicina de Lisboa.

出版信息

Rev Port Cardiol. 1994 Nov;13(11):859-67, 809.

PMID:7848657
Abstract

Heart failure is a pathophysiological state resulting from disturbed cardiac function. It is based on complex molecular processes, many of which are not fully understood. During heart failure adaptive mechanisms, that reinstall altered cardiac function, are activated. The main mechanisms are: a) Alteration of the structure and composition of myocytes by myocardial hypertrophy, reexpression of fetal and neo-natal proteins and the expression of certain proto-oncogenes; b) Activation of the neuroendocrinal system, specifically the sympathetic nervous system, renin-angiotensin-aldosterone system and vasopressin release; c) Activation of autocrine and paracrine systems. However, when these systems are activated beyond a certain limit they contribute to heart failure aggravation. This can also be promoted by alteration of the calcium metabolism inherent in heart failure. The synthesis of the counterregulator atrial natriuretic factor is also increased.

摘要

心力衰竭是一种由心脏功能紊乱导致的病理生理状态。它基于复杂的分子过程,其中许多过程尚未完全被理解。在心力衰竭期间,能够重新恢复改变的心脏功能的适应性机制被激活。主要机制包括:a) 通过心肌肥大、胎儿和新生儿蛋白的重新表达以及某些原癌基因的表达,使心肌细胞的结构和组成发生改变;b) 神经内分泌系统的激活,特别是交感神经系统、肾素 - 血管紧张素 - 醛固酮系统和抗利尿激素的释放;c) 自分泌和旁分泌系统的激活。然而,当这些系统被激活超过一定限度时,它们会导致心力衰竭加重。心力衰竭固有的钙代谢改变也可促进这种情况。反调节因子心房利钠因子的合成也会增加。

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