Cerebral Blood Flow Does Not Adapt to Sustained Hypoxia

Severinghaus et aI. (1966) studied the CBF re­ sponse in humans acclimatizing to the sustained hypoxia of high altitude (3,810 m). Their results in­ dicate that CBF is elevated initially upon ascent to altitude but returns halfway toward sea level values over a period of 4 days. The observations of Sev­ eringhaus et aI. have been interpreted to indicate that there is an of the vasodilator re­ sponse of CBF during sustained hypoxia (Manohar et aI., 1984). By adaptation we mean a progres­ sive failure of cerebral vessels to dilate in response to a sustained hypoxic stimulus. This hypoxic ad­ aptation would be similar to the seen with sustained hypocapnia described by Fencl et al. (1965) and Severinghaus (1965) who termed it resetting (Severinghaus et aI., 1966). Hypocap­ nic adaptation refers to a gradual failure of cere­ bral vessels to respond to the constricting effects of systemic hypocapnia. It is important to recognize, however, that Severinghaus et aI. (1966) do not in any way suggest that CBF adapts to sustained hypoxia. Their findings that there is an abrupt nor­ malization of CBF with oxygen breathing in both acute and sustained hypoxia rather argue against this idea. The authors simply note that this drop in CBF may be attributed either to the gradual rise in arterial P02 or to the decline in Pco2 caused by pro­ gressive hyperventilation. To determine whether CBF does adapt to hypox­ ia per se, it is necessary to control not only arterial P02 but also arterial Pco2 and arterial O2 capacity.