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[肌肉运动增强血流及胰岛素样活性的新方面:激肽释放酶-激肽-前列腺素系统可能的参与(作者译)]

[New aspects of the blood flow-augmenting and insulin-like activity of muscle exercise: possible involvement of the kallikrein-kinin-prostaglandin system (author's transl)].

作者信息

Dietze G

出版信息

Klin Wochenschr. 1982 May 3;60(9):429-44. doi: 10.1007/BF01720357.

Abstract

Adaptations of energy metabolism, as they occur during contractions of skeletal muscle besides by anaerobic glycolysis are achieved via changes in capillary blood flow providing substrates and oxygen for combustion. Since, initially, oxygen supply is restricted in the working muscle, glucose would seem to be the adequate fuel as it may be used anaerobically and yields more energy per mole of oxygen than fatty acids under such circumstances. Besides glucose, amino acids are also required for accelerated proteosynthesis according to the work load. Therefore, an enlargement of the capillary net has to be accompanied by an amplification of the action of insulin, which is often present in only small amounts, e.g., after an overnight fast. This aim is met in three ways: (1) enlargement of the capillary net with accelerated blood flow increasing the supply of insulin and the number of receptor sites for insulin binding; (2) accelerated transport of insulin through the capillary wall, providing more insulin in the interstitial space and at the plasma membranes; (3) a molecular mechanism directly involving the insulin-receptor-messenger complex, localized at the plasma membrane of the working muscle cell. These mechanisms resemble a self-regulatory process, set in motion by the release of metabolites from the working tissue. From recent studies there is accumulating evidence that kinins liberated from their precursors are involved as tissue hormones by carrying the signal across the interstitial space to the smooth muscle cells of the capillary vessels. Concomitantly, prostaglandins are released intracellularly to bring about, in cooperation with kinins, the various adaptive mechanisms. Amplifying systems of this kind may play a role not only in muscle but also in other tissues where adequate kinin or prostaglandin release would appear beneficial under several clinical conditions such as shock, coronary infarction, wound healing, etc.

摘要

除了通过无氧糖酵解外,骨骼肌收缩过程中能量代谢的适应性变化是通过毛细血管血流量的改变来实现的,毛细血管血流量的改变为燃烧提供底物和氧气。由于最初工作肌肉中的氧气供应受到限制,葡萄糖似乎是合适的燃料,因为在这种情况下它可以无氧使用,并且每摩尔氧气产生的能量比脂肪酸更多。除了葡萄糖外,根据工作负荷,加速蛋白质合成还需要氨基酸。因此,毛细血管网的扩大必须伴随着胰岛素作用的增强,而胰岛素的量通常很少,例如在禁食一夜后。这一目标通过三种方式实现:(1)毛细血管网扩大,血流加速,增加胰岛素供应和胰岛素结合受体位点的数量;(2)胰岛素通过毛细血管壁的加速转运,在间质空间和质膜处提供更多胰岛素;(3)一种直接涉及胰岛素-受体-信使复合物的分子机制,定位于工作肌肉细胞的质膜。这些机制类似于一个自我调节过程,由工作组织中代谢产物的释放启动。最近的研究越来越多地表明,从前体释放的激肽作为组织激素参与其中,通过将信号穿过间质空间传递到毛细血管的平滑肌细胞。同时,前列腺素在细胞内释放,与激肽协同作用,引发各种适应性机制。这种放大系统不仅可能在肌肉中起作用,而且在其他组织中也可能起作用,在诸如休克、冠状动脉梗塞、伤口愈合等几种临床情况下,适当释放激肽或前列腺素似乎是有益的。

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