Abstract
During acute hypoxic exposure global cerebral blood flow (gCBF) increases to compensate for the reduced arterial oxygen content (CaO2). Nevertheless, if exposure extends over several days, both CaO2 and gCBF normalize. Hemoconcentration, caused by plasma volume contraction, is the primary mechanism underlying the restoration of CaO2 and could thus also explain the gCBF normalization. Accordingly, we tested the hypothesis that elimination of hypoxia-induced hemoconcentration would return gCBF to acute hypoxia levels. Twenty-three healthy lowlanders (11 males, 24±4 yrs, 65.7±7.4 kg, 1.74±0.1 m) completed two identical four-day sojourns in a hypobaric chamber, one in normoxia (NX) and one in hypobaric hypoxia (HH, corresponding to 3,500 m altitude). During both sojourns, gCBF was measured by duplex ultrasound after 1, 6, 12, 48 and 96 h. An additional measurement was performed at the end of the HH sojourn after normalizing venous hemoglobin concentration ([Hb]) to pre-exposure levels by hypervolemic hemodilution. Compared to NX, gCBF was increased in HH after 1 h (853±173 to 1052±291 ml min−1; p=0.033) and 6 h (839±175 to 955±204 ml min−1; p<.001), but similar on all later time points (all p>0.13). [Hb] increased throughout the HH sojourn (13.7±0.7 to 14.8±1.0 g dl−1; p=<.001) and was restored to pre-sojourn values after hemodilution (13.9±1.1 g dl−1; p=0.27). Contrary to our hypothesis, however, gCBF was unaffected by the hemodilution (974±282 to 872±200 ml min−1, p=0.104). We thus conclude that, at least at this moderate altitude, hemoconcentration is not the primary factor underlying gCBF normalization with acclimatisation. This indicates that CaO2 changes per se are not the principal stimulus for gCBF regulation at altitude.