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猫脑循环中的肾上腺素能受体与血管阻力

Adrenergic receptors and vascular resistance in cerebral circulation of the cat.

作者信息

Muravchick S, Bergofsky E H

出版信息

J Appl Physiol. 1976 May;40(5):797-804. doi: 10.1152/jappl.1976.40.5.797.

Abstract

Infusion of catecholamines and pharmacologic blockade were used to demonstrate the presence of an adrenergic receptor system with both alpha and beta components inthe feline cerebral vasculature. For this purpose, the anatomically isolated brain preparation was perfused under controlled constant-pressure conditions to eliminate active autoregulatory changes and passive fluctuations in calculated cerebral vascular resistance (CVR) secondary to alterations of perfusion pressure. Alpha adrenergic activity was demonstrated as substantial cerebral vasoconstriction in response to infusions of l-norepinephrine and epinephrine; cerebral blood flow (CBF) was decreased by mean values of 25% and 29%, respectively, with calculated increases in CVR of 82% and 62%, respectively. Marked reductions in the vasoconstriction produced by these two catecholamines followed the use of the alpha receptor blocking drug, phenoxybenzamine. Isoproterenol consistently produced cerebral vasodilation (mean CVR decrease of 22%), and this vasodilation was blocked during infusion of a specific beta adrenergic blocking agent, propranolol. Histamine vasodilation (mean CBF increase 49%) appeared to be independent of the classic adrenergic mechanisma. The observed responses are explained on the basis of a functionally significant cerebrovascular adrenergic system having high specificity and demonstrating considerable potency. The data also indicate a predominance of alpha over beta adrenergic cerebrovascular reception.

摘要

通过输注儿茶酚胺和进行药理阻断,来证明猫脑血管系统中存在同时具有α和β成分的肾上腺素能受体系统。为此,在解剖学上分离的脑标本在可控的恒压条件下进行灌注,以消除主动的自动调节变化以及由于灌注压改变而导致的计算脑血流阻力(CVR)的被动波动。α肾上腺素能活性表现为对输注去甲肾上腺素和肾上腺素的显著脑血管收缩反应;脑血流量(CBF)分别平均降低25%和29%,计算得出的CVR分别增加82%和62%。在使用α受体阻断药物酚苄明后,这两种儿茶酚胺产生的血管收缩明显减弱。异丙肾上腺素始终引起脑血管舒张(平均CVR降低22%),并且在输注特异性β肾上腺素能阻断剂普萘洛尔期间,这种血管舒张被阻断。组胺引起的血管舒张(平均CBF增加49%)似乎与经典的肾上腺素能机制无关。观察到的反应是基于一个具有功能重要性、高度特异性且具有相当效力的脑血管肾上腺素能系统来解释的。数据还表明,α肾上腺素能脑血管受体在数量上超过β肾上腺素能脑血管受体。

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