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压力和容量超负荷导致的心肌肥厚:截然不同的生物学现象?

Cardiac hypertrophy due to pressure and volume overload: distinctly different biological phenomena?

作者信息

Rossi M A, Carillo S V

机构信息

Department of Pathology, Faculty of Medicine of Ribeirão Preto, University of São Paulo, Brazil.

出版信息

Int J Cardiol. 1991 May;31(2):133-41. doi: 10.1016/0167-5273(91)90207-6.

Abstract

Myocardial hypertrophy is a morphological adaptive response to chronic work overload imposed on the heart. It has been categorized into two distinct basic types: concentric hypertrophy, occurring in response to a sustained pressure overload in which wall thickness increases without chamber enlargement, and eccentric hypertrophy, in response to a chronic volume overload in which chamber volume enlarges without a relative increase in its wall thickness. It should be emphasized, in this context, that these adjectives are somewhat confusing, since the hypertrophy observed is not eccentric in the fashion often seen in the left ventricle of patients with hypertrophic cardiomyopathy. In fact, the hypertrophy is concentric in both instances, but is associated with an increase in chamber volume when described as eccentric, yet occurring with a maintained volume when said to be concentric. In rats made anemic by iron deficiency, the volume overloaded heart achieves an adaptive increase in mass characterized as hypertrophy occurring in the setting of dilated ventricle. This so-called eccentric hypertrophy depends on catecholamines as possible signals for myocardial growth, and progresses with preserved ultrastructure and contractile performance of the cardiac muscle. A gradually imposed volume overload results in a harmonious growth of the heart (it retains a relative normal shape, becoming a magnified normal heart), probably mediated by release of catecholamines into the myocardium. This process resembles the normal cardiac growth in response to the obligatory volume load imposed by an increasing cardiac output (greater metabolic demands) and blood volume.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

心肌肥厚是心脏对慢性工作负荷过重的一种形态学适应性反应。它已被分为两种不同的基本类型:向心性肥厚,发生于对持续压力负荷过重的反应中,此时心室壁厚度增加而腔室大小不变;离心性肥厚,发生于对慢性容量负荷过重的反应中,此时腔室容积增大而其壁厚度无相对增加。在此背景下应强调的是,这些形容词有点令人困惑,因为观察到的肥厚并非肥厚型心肌病患者左心室中常见的那种离心性。事实上,在这两种情况下肥厚都是向心性的,但当被描述为离心性时与腔室容积增加相关,而当被称为向心性时则在容积保持的情况下发生。在缺铁导致贫血的大鼠中,容量负荷过重的心脏实现了质量的适应性增加,其特征为在扩张心室情况下发生的肥厚。这种所谓的离心性肥厚依赖儿茶酚胺作为心肌生长的可能信号,并在心肌超微结构和收缩性能得以保留的情况下进展。逐渐施加的容量负荷过重会导致心脏的协调生长(它保持相对正常的形状,成为放大的正常心脏),这可能是由儿茶酚胺释放到心肌中所介导的。这个过程类似于心脏对因心输出量增加(更大的代谢需求)和血容量增加所施加的必要容量负荷的正常生长。(摘要截短于250词)

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