氟烷诱导的大鼠脑突触体膜流动性改变及其与麻醉的关系。

Halothane-induced alteration in the fluidity of rat brain synaptosomal membranes and its relationship to anesthesia.

作者信息

Sastry B V, Franks J J, Surber M J

机构信息

Department of Pharmacology, Vanderbilt University School of Medicine, Nashville, Tennessee 37232-6600.

出版信息

Ann N Y Acad Sci. 1991;625:433-7. doi: 10.1111/j.1749-6632.1991.tb33872.x.

DOI:10.1111/j.1749-6632.1991.tb33872.x

PMID:2058898

Abstract

Concentrations of halothane 1.43% or higher abolished the pain response and induced anesthesia. Halothane increased membrane fluidity of synaptosomes and microsomes both at non-anesthetic and anesthetic concentrations. Changes in fluidity in synaptosomes did not return to control levels even after the animals recovered from anesthesia. Alteration in membrane fluidity by halothane is a non-selective effect and may not play a definitive role in anesthesia.

摘要

氟烷浓度达到1.43%或更高时可消除疼痛反应并诱导麻醉。在非麻醉浓度和麻醉浓度下，氟烷均可增加突触体和微粒体的膜流动性。即使动物从麻醉中恢复后，突触体的流动性变化也未恢复到对照水平。氟烷引起的膜流动性改变是一种非选择性效应，可能在麻醉中不发挥决定性作用。