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Rate of calcium binding and uptake in normal animal and failing human cardiac muscle. Membrane vesicles (relaxing system) and mitochondria.正常动物和衰竭人类心肌中钙结合与摄取的速率。膜囊泡(舒张系统)和线粒体。
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细胞内钙处理在人心室心肌力-间期关系中的作用

Role of intracellular calcium handling in force-interval relationships of human ventricular myocardium.

作者信息

Gwathmey J K, Slawsky M T, Hajjar R J, Briggs G M, Morgan J P

机构信息

Charles A. Dana Research Institute, Beth Israel Hospital, Boston, Massachusetts 02215.

出版信息

J Clin Invest. 1990 May;85(5):1599-613. doi: 10.1172/JCI114611.

DOI:10.1172/JCI114611
PMID:2332508
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC296612/
Abstract

Experiments were performed in human working myocardium to investigate the relationship of intracellular calcium handling and availability to alterations in the strength of contraction produced by changes in stimulation rate and pattern. Both control and myopathic muscles exhibited potentiation of peak isometric force during the postextrasystolic contraction which was associated with an increase in the peak intracellular calcium transient. Frequency-related force potentiation was attenuated in myopathic muscles compared to controls. This occurred despite an increase in resting intracellular calcium and in the peak amplitude of the calcium transient as detected with aequorin. Therefore, abnormalities in contractile function of myopathic muscles during frequency-related force potentiation are not due to decreased availability of intracellular calcium, but more likely reflect differences in myofibrillar calcium responsiveness. Sarcolemmal calcium influx may also contribute to frequency-related changes in contractile force in myopathic muscles as suggested by a decrease in action potential duration with increasing stimulation frequency which is associated with fluctuations in peak calcium transient amplitude.

摘要

在人体工作心肌中进行了实验,以研究细胞内钙处理和可利用性与刺激速率和模式变化所产生的收缩强度改变之间的关系。对照肌肉和病变肌肉在早搏后收缩期间均表现出等长峰值力的增强,这与细胞内钙瞬变峰值的增加有关。与对照相比,病变肌肉中频率相关的力增强减弱。尽管用发光蛋白检测到静息细胞内钙增加以及钙瞬变的峰值幅度增加,但仍出现这种情况。因此,病变肌肉在频率相关的力增强过程中收缩功能的异常并非由于细胞内钙的可利用性降低,而更可能反映了肌原纤维钙反应性的差异。肌膜钙内流也可能导致病变肌肉中收缩力的频率相关变化,这一点由动作电位持续时间随刺激频率增加而减少所暗示,而这与钙瞬变峰值幅度的波动有关。