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胶原蛋白基质对离体大鼠心脏左心室被动力学的作用。

Contribution of collagen matrix to passive left ventricular mechanics in isolated rat hearts.

作者信息

MacKenna D A, Omens J H, McCulloch A D, Covell J W

机构信息

Department of Medicine (Cardiology), University of California, San Diego, La Jolla 92093.

出版信息

Am J Physiol. 1994 Mar;266(3 Pt 2):H1007-18. doi: 10.1152/ajpheart.1994.266.3.H1007.

DOI:10.1152/ajpheart.1994.266.3.H1007
PMID:8160804
Abstract

Although it makes up only 2-6% of left ventricular dry weight, collagen is thought to be the major structural protein determining passive ventricular stiffness. However, the relationship between structure of the extracellular matrix and passive mechanics is not understood. Hence, to deplete the collagen matrix, 16 rat hearts were perfused with bacterial collagenase for 60 min. Quantitative morphology using picrosirius red revealed a 36% decrease in collagen area fraction predominantly in the medium-sized fibers. Scanning electron microscopy revealed damage to the endomysial struts. Passive pressure-volume curves showed increases in left ventricular volume at all pressures (from 0.203 +/- 0.061 to 0.265 +/- 0.061 ml at 5 mmHg, P < 0.0001). Strain during loading, calculated from lengths obtained from a triplet of piezoelectric crystals, was unchanged with collagen depletion. However, remodeling strain computed from the collagenase-treated state referred to the Krebs solution-treated state at the same ventricular pressure showed both circumferential (0.145 +/- 0.166 to 0.170 +/- 0.158) and longitudinal (0.070 +/- 0.120 to 0.068 +/- 0.069) stretching. Sarcomere lengths increased at all depths (5.2% at midwall). Thus alterations in the extracellular matrix lead to increased ventricular volume and sarcomere lengths without altering ventricular compliance.

摘要

尽管胶原蛋白仅占左心室干重的2%-6%,但它被认为是决定心室被动僵硬度的主要结构蛋白。然而,细胞外基质结构与被动力学之间的关系尚不清楚。因此,为了去除胶原蛋白基质,对16只大鼠心脏灌注细菌胶原酶60分钟。使用苦味酸天狼星红进行的定量形态学分析显示,胶原蛋白面积分数主要在中等大小纤维中减少了36%。扫描电子显微镜显示肌内膜支柱受损。被动压力-容积曲线显示,在所有压力下左心室容积均增加(5 mmHg时从0.203±0.061 ml增加到0.265±0.061 ml,P<0.0001)。由一组压电晶体获得的长度计算得出的加载过程中的应变,在胶原蛋白减少时未发生变化。然而,根据胶原酶处理状态相对于相同心室压力下的克雷布斯溶液处理状态计算得出的重塑应变显示,圆周方向(从0.145±0.166到0.170±0.158)和纵向方向(从0.070±0.120到0.068±0.069)均有拉伸。肌节长度在所有深度均增加(中壁处增加5.2%)。因此,细胞外基质的改变导致心室容积和肌节长度增加,而不改变心室顺应性。

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