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缺氧和复氧挛缩期间的心肌僵硬度。

Myocardial stiffness during hypoxic and reoxygenation contracture.

作者信息

Lewis M J, Housmans P R, Claes V A, Brutsaert D L, Henderson A H

出版信息

Cardiovasc Res. 1980 Jun;14(6):339-44. doi: 10.1093/cvr/14.6.339.

Abstract

Isolated rat papillary muscle preparations were used to study hypoxic contracture, and cat papillary muscle preparations with ouabain to study reoxygenation contracture. Electronic analysis of the response to rapid small sinusoidal perturbations gave a continuous measurement of the elastic and viscous components of total stiffness. Increased resting force during hypoxic contracture was characterised by an increase in resting elastic and viscous stiffness relative to the control stiffness-active force relationships. During reoxygenation contracture the stiffness-force relationships followed those of active force development. The linear active force-elastic stiffness relationship (dt/dl=kT+c) was also reversibly altered during hypoxic contracture, predominantly by an increase in intercept c. These data imply that hypoxic contracture unlike reoxygenation contracture is not due solely to a rise in intracellular calcium, but is associated with a component of stiffness not participating an active force development, for example rigor.

摘要

使用离体大鼠乳头肌标本研究缺氧性挛缩,使用含有哇巴因的猫乳头肌标本研究复氧性挛缩。对快速小正弦扰动反应的电子分析可连续测量总刚度的弹性和粘性成分。缺氧性挛缩期间静息力增加的特征是,相对于对照刚度-主动力关系,静息弹性和粘性刚度增加。在复氧性挛缩期间,刚度-力关系遵循主动力发展的关系。线性主动力-弹性刚度关系(dt/dl=kT+c)在缺氧性挛缩期间也发生可逆变化,主要是截距c增加。这些数据表明,与复氧性挛缩不同,缺氧性挛缩并非仅由细胞内钙升高引起,而是与不参与主动力发展的刚度成分有关,例如强直收缩。

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