Rol' oksida azota v tserebral'noi vazokonstriktsii u krys pri dykhanii kislorodom pod davleniiem.

I. T. Demchenko, A. E. Bosso, S. I. Zhiliaev, A. N. Moskvin, D. R. Gutsaeva, D. N. Atochin, P. B. Bennett, K. A. Piantadossi

Результат исследований: Материалы для журналаСтатьярецензирование

9 Цитирования (Scopus)

Аннотация

High pressure oxygen evokes a cerebral vasoconstriction and diminishes cerebral blood flow with the aid of mechanisms which are not yet sufficiently studied. We were checking a hypothesis that the hyperbaric oxygen (HBO2) inactivates cerebral nitrogen oxide (NO), interrupts its basal relaxing effect, and evokes a vasoconstriction. In our experiments, HBO2 decreased cerebral blood flow depending on the pressure. Inhibiting the NO-synthase weakened basal vasorelaxation in breathing with atmosphere air and eliminated the vasoconstriction in exposure to the HBO2. Inactivation of O2 prevented the HBO2-induced vasoconstriction. The data obtained reveal that diminishing of cerebral blood flow in HBO is related to the NO inactivation and weakening of its basal vasorelaxing effect. Possible mechanisms of the NO inactivation may involve its reaction with oxygen and superoxide anion which lead to diminishing of the tissue NO concentration and weakening of its vasorelaxing effect.

Переведенное названиеInvolvement of nitrogen oxide in the cerebral vasoconstriction during respiration with high pressure oxygen
Язык оригиналаРусский
Страницы (с-по)1594-1603
Число страниц10
ЖурналRossiiskii fiziologicheskii zhurnal imeni I.M. Sechenova / Rossiiskaia akademiia nauk
Том86
Номер выпуска12
СостояниеОпубликовано - дек 2000
Опубликовано для внешнего пользованияДа

ASJC Scopus subject areas

  • Physiology

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