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肥厚型大鼠左心室结构蛋白与收缩蛋白重塑及心肌僵硬度

Structural vs. contractile protein remodeling and myocardial stiffness in hypertrophied rat left ventricle.

作者信息

Jalil J E, Doering C W, Janicki J S, Pick R, Clark W A, Abrahams C, Weber K T

机构信息

Cardiovascular Institute, Michael Reese Hospital, University of Chicago Pritzker School of Medicine, IL 60616.

出版信息

J Mol Cell Cardiol. 1988 Dec;20(12):1179-87. doi: 10.1016/0022-2828(88)90597-4.

DOI:10.1016/0022-2828(88)90597-4
PMID:2470910
Abstract

Left ventricular pressure overload will result in the hypertrophic growth of the myocardium and in the rat may include a remodeling of both the structural and contractile proteins. As a result, an adaptive rise in active stiffness, or the force generating capacity of the myocardium, may occur. The relative importance of structural vs. contractile protein remodeling to the hypertrophic response and active stiffness is unclear. Accordingly, we monitored the ratio of V1/V3 isomyosin and the fibrillar nature and volume fraction of myocardial collagen, together with the developed systolic stress-strain relation of the intact myocardium in the adult male Wistar rat after 8 weeks of abdominal aorta banding. In comparison to controls and for the 20% increase in left ventricular mass obtained with banding we found: (a) collagen volume fraction had increased significantly (6.2 +/- 2.0 vs. 3.6 +/- 1.0%) while the V1/V3 ratio did not change; (b) interstitial compartment remodeling included a perivascular accumulation of collagen around small intramyocardial coronary arteries and the appearance of more extensive fibrillar collagens; and (c) active stiffness increased significantly. Thus, the increase in active stiffness of the hypertrophied adult rat myocardium, seen with abdominal aorta banding, appears to be related to interstitial fibrosis and not a conversion of myosin isoforms.

摘要

左心室压力超负荷会导致心肌肥厚性生长,在大鼠中可能包括结构蛋白和收缩蛋白的重塑。结果,心肌的主动僵硬度或产生力的能力可能会适应性升高。结构蛋白与收缩蛋白重塑对肥厚反应和主动僵硬度的相对重要性尚不清楚。因此,我们监测了V1/V3同工型肌球蛋白的比例、心肌胶原的纤维性质和体积分数,以及成年雄性Wistar大鼠腹主动脉结扎8周后完整心肌的收缩期应力-应变关系。与对照组相比,结扎导致左心室质量增加20%,我们发现:(a)胶原体积分数显著增加(6.2±2.0%对3.6±1.0%),而V1/V3比例没有变化;(b)间质区重塑包括心肌内小冠状动脉周围血管周围胶原的积聚和更广泛的纤维状胶原的出现;(c)主动僵硬度显著增加。因此,腹主动脉结扎所见的成年大鼠肥厚心肌主动僵硬度的增加似乎与间质纤维化有关,而不是肌球蛋白同工型的转变。

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