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骨骼肌交感神经血管反应中的β-肾上腺素能扩张成分。对微循环和跨毛细血管交换的影响。

Beta adrenergic dilator component of the sympathetic vascular response in skeletal muscle. Influence on the micro-circulation and on transcapillary exchange.

作者信息

Lundvall J, Järhult J

出版信息

Acta Physiol Scand. 1976 Feb;96(2):180-92. doi: 10.1111/j.1748-1716.1976.tb10187.x.

Abstract

A neurogenic beta-adrenergic vasodilatation in skeletal muscle has been indicated by some recent investigations. The present study describes the extent to which this neurogenic beta-dilator mechanism contributes to the integrated vascular response in consecutive sections of the muscle vascular bed during sympathetic nerve activation. This was done by studying the vascular reactions to graded sympathetic stimulation (1-16 Hz) before and after beta-adrenoceptor blockade. Beta-blockade did not influence significantly the sympathetically induced changes of total muscle vascular resistance or capacitance. Vascular tone in the "micro-vessels" during stimulation was, however, clearly more pronounced in the beta-blocked than in the non-blocked region, as revealed by segmental resistance analysis and by determination of precapillary sphincter tone (CFC). In addition, beta-blockade markedly reduced the net transcapillary absorption of extravascular fluid evoked by nerve activation. This effect could be ascribed to the mentioned influence on the precapillary sphincters, leading to a decrease of the number of capillaries available for transcapillary exchange, and to a limitation of the nerve induced fall of capillary hydrostatic pressure. The described effects of alpha-blockade were observed at all rates of sympathetic stimulation.--The conclusion was reached that the beta-adrenergic dilator component of the sympathetic vascular response in skeletal muscle significantly modifies the alpha-adrenergic constriction in the micro-vessels. It is suggested that, in the intact organism, this neurogenic beta-dilator mechanism is primarily aimed at improving the transcapillary exchange.

摘要

最近的一些研究表明,骨骼肌中存在神经源性β - 肾上腺素能血管舒张。本研究描述了在交感神经激活期间,这种神经源性β - 舒张机制对肌肉血管床连续节段中血管综合反应的贡献程度。这是通过研究β - 肾上腺素能受体阻断前后对分级交感神经刺激(1 - 16赫兹)的血管反应来实现的。β - 受体阻断对交感神经诱导的总肌肉血管阻力或容量的变化没有显著影响。然而,通过节段阻力分析和毛细血管前括约肌张力(CFC)测定发现,刺激期间“微血管”中的血管张力在β - 受体阻断区域比未阻断区域明显更显著。此外,β - 受体阻断显著降低了神经激活引起的血管外液净毛细血管吸收。这种效应可归因于上述对毛细血管前括约肌的影响,导致可用于毛细血管交换的毛细血管数量减少,以及神经诱导的毛细血管流体静压下降受到限制。在所有交感神经刺激速率下均观察到了所述的α - 受体阻断效应。得出的结论是,骨骼肌中交感神经血管反应的β - 肾上腺素能舒张成分显著改变了微血管中的α - 肾上腺素能收缩。有人提出,在完整机体中,这种神经源性β - 舒张机制主要旨在改善毛细血管交换。

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