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依诺昔酮对豚鼠右心室乳头肌力学和能量学的影响。

Influence of enoximone on mechanics and energetics of right ventricular guinea pig papillary muscles.

作者信息

Holubarsch C, Hasenfuss G, Just H, Blanchard E, Mulieri L A, Alpert N R

机构信息

Department of Cardiology, University of Freiburg, F.R.G.

出版信息

J Cardiovasc Pharmacol. 1989;14 Suppl 1:S24-8.

PMID:2480481
Abstract

Using highly sensitive antimony-bismuth thermopiles, the heat that is liberated during isometric contraction (initial heat) was measured simultaneously with the force signal in right ventricular papillary muscles of guinea pigs (n = 10). Measurements were taken before and after application of enoximone in a concentration of 10(-5) M. Enoximone increased peak developed tension from 1.92 +/- 0.98 to 2.81 +/- 1.11 g/mm2 (p less than 0.01) and the tension-time integral from 1.52 +/- 0.87 to 1.86 +/- 0.86 g.s/mm2 (p less than 0.05). Initial heat was increased from 0.50 +/- 0.13 to 0.79 +/- 0.24 mcal/g (p less than 0.01). The ratio between initial heat and tension-time integral, which is an inverse measure of myocardial economy of force generation, was increased from 3.77 +/- 1.17 to 4.66 +/- 1.49 mucal/g.s.cm (p less than 0.05). To study the potential changes induced by enoximone on an intracellular level, the initial heat was separated into tension-dependent heat (cross-bridge cycling) and tension-independent heat (calcium cycling). The latter increased from 0.20 +/- 0.05 to 0.28 +/- 0.09 mcal/g (p less than 0.05). The tension-dependent heat as normalized for a unit of developed tension-time integral increased from 2.17 +/- 0.63 to 2.86 +/- 0.79 mucal/g.s.cm (p less than 0.01). From these data, we conclude that enoximone decreases the economy of myocardial force generation by (a) increasing the number of calcium ions cycling during one twitch and (b) by altering the fundamental mechanisms of the contractile proteins with respect to force generation, i.e., faster contraction velocity and decreased economy of force generation.

摘要

使用高灵敏度的锑铋热电堆,在豚鼠(n = 10)右心室乳头肌中,等长收缩期间释放的热量(初始热)与力信号同时进行测量。在施加浓度为10(-5) M的依诺昔酮前后进行测量。依诺昔酮使峰值张力从1.92±0.98增加到2.81±1.11 g/mm2(p<0.01),张力-时间积分从1.52±0.87增加到1.86±0.86 g.s/mm2(p<0.05)。初始热从0.50±0.13增加到0.79±0.24 mcal/g(p<0.01)。初始热与张力-时间积分的比值,这是心肌产生力的经济性的反向指标,从3.77±1.17增加到4.66±1.49 mucal/g.s.cm(p<0.05)。为了研究依诺昔酮在细胞内水平引起的潜在变化,将初始热分为张力依赖性热(横桥循环)和张力非依赖性热(钙循环)。后者从0.20±0.05增加到0.28±0.09 mcal/g(p<0.05)。以单位张力-时间积分归一化的张力依赖性热从2.17±0.63增加到2.86±0.79 mucal/g.s.cm(p<0.01)。从这些数据中,我们得出结论,依诺昔酮通过以下方式降低心肌产生力的经济性:(a)增加一次抽搐期间循环的钙离子数量,以及(b)改变收缩蛋白在产生力方面的基本机制,即更快的收缩速度和降低的产生力的经济性。

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