Abstract
CBF increases with acute hypoxia despite the opposing vasoconstrictor effects of the drop in pCO2 caused by hyperventilation. Maintaining normocapnia by adding CO2 the hypoxic CBF responsiveness about doubles. As we have shown recently by this test, the hypoxic CBF response is not blunted but rather somewhat sharpened over five days at almost 4000 meters of altitude. This, along with other evidence, shows that CBF does not in itself adapt to chronic hypoxia. Nevertheless, a decrease in CBF is seen over days at constant altitude primarily due to increase in the hematocrit. The cerebral vasodilatation cannot explain the usual (mild) form of AMS. But it may well be involved in the pathogenesis of the rare but severe cerebral form of AMS, as prolonged increased capillary pressure in vasodilated areas could lead to vasogenic cerebral edema.

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