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兔体内胆碱能性脑血管舒张:缺乏伴随的代谢激活。

Cholinergic cerebral vasodilatation in the rabbit: absence of concomitant metabolic activation.

作者信息

Scremin O U, Sonnenschein R R, Rubinstein E H

出版信息

J Cereb Blood Flow Metab. 1982;2(2):241-7. doi: 10.1038/jcbfm.1982.24.

DOI:10.1038/jcbfm.1982.24
PMID:6804471
Abstract

Cerebral blood flow (CBF) was estimated from measurements of internal carotid blood flow and sagittal sinus blood flow in mechanically ventilated rabbits under 70% N2O-30% O2. Intravenously administered physostigmine, a cholinesterase inhibitor, increased CBF under normocapnia and enhanced the cerebral vasodilatation of hypercapnia, but did not alter the cerebral metabolic rate of oxygen (CMRO2). The cerebrovascular effects of physostigmine were antagonized by atropine but not by dihydro-beta-erythroidine, a nicotinic blocker. Neostigmine, a quaternary cholinesterase inhibitor that does not cross the blood-brain barrier, showed no cerebrovascular effects. It is concluded that the cholinergic cerebral vasodilatation does not depend on cerebral metabolic activation, and that the cholinergic receptors involved are muscarinic and located beyond the blood-brain barrier.

摘要

在70%氧化亚氮-30%氧气条件下,对机械通气的家兔进行颈内动脉血流和矢状窦血流测量,以此估算脑血流量(CBF)。静脉注射胆碱酯酶抑制剂毒扁豆碱,在正常碳酸血症时可增加CBF,并增强高碳酸血症时的脑血管舒张,但不改变脑氧代谢率(CMRO2)。毒扁豆碱的脑血管效应可被阿托品拮抗,但不能被烟碱阻断剂二氢-β-刺桐啶拮抗。新斯的明是一种不能透过血脑屏障的季铵类胆碱酯酶抑制剂,未显示出脑血管效应。得出的结论是,胆碱能性脑血管舒张不依赖于脑代谢激活,且所涉及的胆碱能受体为毒蕈碱型,位于血脑屏障之外。

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