[大脑中的高氧性血管收缩是通过超氧阴离子使一氧化氮失活来实现的]

[Hyperoxic vasoconstriction in the brain is realized by inactivation of nitric oxide by superoxide anions].

作者信息

Zhiliaev S Iu, Moskvin A N, Platonova T F, Gutsaeva D R, Churilina I V, Demchenko I T

机构信息

I. M. Sechenov Institute of Evolutionary Physiology and Biochemistry, Russian Acad. Sci., 194223, St. Petersburg, pr. M. Toreza, 44, Russia.

出版信息

Ross Fiziol Zh Im I M Sechenova. 2002 May;88(5):553-9.

PMID:12136722

Abstract

We tested a hypothesis that the cerebral blood flow (CBF) is reduced at hyperbaric oxygen due to inactivation of nitric oxide (NO) by superoxide anions (O2). In our experiments, the CBF was measured under hyperbaric oxygenation (HBO) 4ATA after inhibition of NO synthesis and inactivation of O2. The CBF was reduced at HBO exposure. Inhibition of NO--synthase type I and III (NOS) by L-NAME in the air caused the same decreasing of the CBF as at 4 ATA HBO. Hyperbaric vasoconstriction was diminished after NOS inhibition. Intravenous injection of superoxide dismutase (CuZn SOD) increased the CBF in the air and HBO exposure. This effect disappeared at preliminary NOS inhibition. These data suggest that inactivation of NO by O2 is a more effective mechanism of HBO vasoconstriction.

摘要

我们检验了一个假设，即高压氧环境下脑血流量（CBF）会因超氧阴离子（O₂）使一氧化氮（NO）失活而降低。在我们的实验中，在抑制NO合成和使O₂失活后，于4ATA高压氧合（HBO）条件下测量CBF。暴露于HBO时CBF降低。在空气中L-NAME抑制I型和III型一氧化氮合酶（NOS）导致CBF出现与4ATA HBO时相同程度的降低。抑制NOS后高压性血管收缩减弱。静脉注射超氧化物歧化酶（CuZn SOD）可增加空气中及HBO暴露时的CBF。在预先抑制NOS后这种效应消失。这些数据表明O₂使NO失活是HBO血管收缩更有效的机制。