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出血期间骨骼肌阻力血管中β-肾上腺素能扩张剂与收缩反应的相互作用。

Beta-adrenergic dilator interaction with the constrictor response in resistance vessels of skeletal muscle during hemorrhage.

作者信息

Hillman J, Lundvall J

出版信息

Acta Physiol Scand. 1980 Jan;108(1):77-83. doi: 10.1111/j.1748-1716.1980.tb06502.x.

Abstract

A marked beta-adrenergic dilator interaction with the vasoconstrictor response in skeletal muscle during hemorrhage is described. The dilator influence corresponded to some 40% of the constrictor response both at mild and moderate as well as at large bleeding. In absolute resistance units, the beta-adrenergic dilator influence averaged no less than 14 mmHg/ml X min-1 X 100 g-1) at large bleeding (hemorrhagic hypotension of 50 mmHg). Comparison of the hemorrhage induced resistance effects in the autoperfused innervated muscle, in the autoperfused denervated muscle, and in the innervated muscle cross-circulated from a donor animal, showed that the beta-adrenergic dilator influence more or less completely was caused by blood-borne catecholamines, in all likelihood by adrenaline, which is known to be secreted in large amounts during hemorrhage. The described beta-adrenergic dilator mechanism may serve to maintain nutritional blood flow by counteracting the constrictor response. It deserves consideration also from the point of view that it obviously has to be taken into account for proper evaluation of other vascular control mechanisms brought into action in hemorrhage.

摘要

本文描述了在出血期间骨骼肌中β - 肾上腺素能扩张剂与血管收缩反应之间显著的相互作用。无论是轻度和中度出血还是大量出血时,扩张剂的影响约占收缩反应的40%。以绝对阻力单位计算,在大量出血(出血性低血压达50 mmHg)时,β - 肾上腺素能扩张剂的影响平均不少于14 mmHg/ml×min⁻¹×100 g⁻¹)。对自灌注的有神经支配肌肉、自灌注的去神经支配肌肉以及与供体动物交叉循环的有神经支配肌肉中出血诱导的阻力效应进行比较,结果表明,β - 肾上腺素能扩张剂的影响或多或少完全是由血源性儿茶酚胺引起的,很可能是由肾上腺素引起的,已知在出血期间肾上腺素会大量分泌。所描述的β - 肾上腺素能扩张机制可能通过抵消收缩反应来维持营养性血流。从在评估出血时起作用的其他血管控制机制时显然必须考虑这一点来看,它也值得关注。

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