РЕАКЦИИ ЦЕРЕБРАЛЬНЫХ МИКРОСОСУДОВ НА ОСТРОЕ ГИПОКСИЧЕСКОЕ ВОЗДЕЙСТВИЕ ПРИ ЭКЗОГЕННОМ ПОВЫШЕНИИ УРОВНЯ ИНТЕРЛЕЙКИНА-1β В КРОВИ

The peculiarities of the influence of the increased systemic level of the proinflammatory cytokine interleukin-1 beta (IL-1β) on the vasomotor reactions of the pial arterioles of the parietal region of the cerebral cortex of the narcotized rat were studied by progressively developing acute normobaric hypoxia leading to respiratory arrest in apnea and post-hypoxic period. It was shown that the vasodilating effect of hypoxia on the microcirculatory bed of the rat cerebral cortex occurs only with a significant decrease in the oxygen content in the inhaled gas mixture. A significant increase in the diameter of the pial arterioles by 45—55 % was observed in the experimental group of animals that had previously been given an intravenous injection of 500 ng IL-1β with a decrease in the oxygen content in the respiratory mixture to 10 %, whereas in the control group, the diameter of arterioles for a given degree of hypoxia was not changed. When the hypoxia deepened to 4—6 %, which caused respiratory arrest, vasodilation of the pial arterioles was also observed in the control group, reaching 26 %. After the transition to respiration by air, spontaneous respiration was observed in all animals in the control. In the experimental group, in 50 % of the animals, respiration was not restored. Vasodilatation was more pronounced in all animals of the experimental group: the diameter of arterioles increased by 70 % in animals with subsequent complete respiration and 135 % in animals without its restoration. Thus, it has been established that the exogenous increase in the systemic level of IL-1β enhances the sensitivity of the brain microvessels to hypoxia and increases their dilatation in response to a progressively increasing hypoxic effect, while reducing the possibility of spontaneous resumption of respiration after apnea.