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- W122553987 abstract "Publisher SummaryThis chapter discusses the effect of arterial hypoxemia on cerebral blood vessels. Hypoxemia produces cerebral vasodilation and an increase in cerebral blood flow (CBF). However, the precise mechanism by which hypoxemia produces vasodilation is unclear. There is evidence that low PO2 act directly on cerebral vascular smooth muscle, resulting in vasodilation. It has also been suggested that other local factors such as cerebral parenchymal acidosis secondary to anaerobic metabolism and adenosine release caused by hypoxemia are responsible for cerebral dilation. Neurogenic mechanisms are involved in the cerebral vasodilator response to hypoxemia, and it has been suggested that the carotid chemoreceptor is responsible for all, or at least a major part, of the cerebral vasodilation in response to hypoxemia. The the cerebral vasodilation to hypoxemia is not affected by denervation of the carotid or aortic chemoreceptor and is not modified by the denervation of the carotid or aortic baroreceptor. Data suggests that arterial oxygen content is important than arterial oxygen tension in the mechanism of cerebral vasodilation. This chapter presents a study to test the hypothesis that oxygen substrates such as metyrapone and imipramine could alter the responses of the cerebral vasculature to hypoxemia." @default.
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- W122553987 date "1981-01-01" @default.
- W122553987 modified "2023-09-27" @default.
- W122553987 title "A POSSIBLE ROLE OF OXYGENASES IN THE REGULATION OF CEREBRAL BLOOD FLOW" @default.
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- W122553987 doi "https://doi.org/10.1016/b978-0-08-026821-7.50025-7" @default.
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