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大鼠心肌代谢阻滞诱导挛缩的力学和结构相关性

Mechanical and structural correlates of contracture induced by metabolic blockade in cardiac muscle from the rat.

作者信息

Bing O H, Fishbein M C

出版信息

Circ Res. 1979 Aug;45(2):298-308. doi: 10.1161/01.res.45.2.298.

Abstract

We performed morphological studies of myocardial contracture to define its nature and relationship to mechanical changes occurring during metabolic blockade. Isolated rat papillary and trabecular muscles were stretched to the apices of their length-tension curves and stimulated to contract isometrically 12 times a minute at a temperature of 28 degrees C. Incomplete and total metabolic blockade were induced by 1 hour of hypoxia (95% N2, 5% CO2) or by hypoxia plus glycolytic blockade with iodoacetic acid, 10-4M, respectively. In oxygenated control preparations, mechanical performance was stable for the 60-minute experimental period. In preparations exposed to hypoxia, developed tension fell to 7 +/- 2% of prehypoxia values at 60 minutes. Contracture tension increased progressively to 2.5 +/- 0.4 g/mm2. With total metabolic blockade, developed tension declined to zero by 10 minutes, contracture tension rose to an average peak value of 5.3 +/- 0.4 g/mm2 by 15 minutes, and subsequently slowly declined. All preparations were fixed at Lmax in the muscle bath. Light and electron microscopic studies revealed focal irregularities of A, I, and Z bands with sarcomere malalignment, hypercontraction, and fiber disruption, which increased in severity with increasing metabolic blockade. Linear densities appeared in mitochondria following total metabolic blockade, but mitochondria appeared normal otherwise. Thus, myocardial contracture after metabolic blockade is a focal process beginning within the sarcomere; morphological alterations in the contractile apparatus correlate with mechanical changes and are more severe than those in the mitochondria.

摘要

我们对心肌挛缩进行了形态学研究,以确定其本质以及与代谢阻断期间发生的力学变化之间的关系。将离体大鼠乳头肌和小梁肌拉伸至其长度 - 张力曲线的顶点,并在28℃的温度下以每分钟12次的频率刺激其进行等长收缩。分别通过1小时的缺氧(95% N₂,5% CO₂)或缺氧加10⁻⁴M碘乙酸的糖酵解阻断诱导不完全和完全代谢阻断。在有氧的对照制剂中,在60分钟的实验期内力学性能稳定。在暴露于缺氧的制剂中,60分钟时发展张力降至缺氧前值的7±2%。挛缩张力逐渐增加至2.5±0.4 g/mm²。在完全代谢阻断时,发展张力在10分钟时降至零,挛缩张力在15分钟时升至平均峰值5.3±0.4 g/mm²,随后缓慢下降。所有制剂均在肌肉浴中固定于Lmax。光镜和电镜研究显示A带、I带和Z带存在局灶性不规则,伴有肌节排列紊乱、过度收缩和纤维破坏,且随着代谢阻断程度的增加,严重程度增加。完全代谢阻断后线粒体出现线性密度,但线粒体在其他方面看起来正常。因此,代谢阻断后的心肌挛缩是一个始于肌节内的局灶性过程;收缩装置的形态学改变与力学变化相关,且比线粒体中的改变更严重。

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