Intracranial pressures and O2 extraction in conscious sheep during 72 h of hypoxia.

High-altitude cerebral edema may occur within several days after a rapid ascent to altitude. However, the mechanisms that produce this potentially lethal condition are unclear. This experiment assessed systemic arterial and intracranial pressures (n = 22) and cerebral blood flow per unit cerebral O2 consumption (Qc/cVo2) and cerebral O2 extraction fraction (cEo2) (n = 9) in conscious sheep before and during 72 h of normobaric hypoxia (arterial O2 tension approximately 40 mmHg, oxygen saturation in arterial blood approximately 50%). Qc/cVo2 and cEo2 were calculated from systemic arterial and cerebral venous O2 contents. Wet-to-dry brain weight ratios were calculated during normoxia (n = 4) or after 72 h of hypoxia (n = 5) in additional sheep. Intracranial pressures did not change during hypoxia (+ 1.3 to +1.8 mmHg, P = 1.0); however, estimated intracranial capillary hydrostatic pressure may have increased 1-20 mmHg depending on the arterial-to-downstream resistance ratio. During the 72 h of hypoxia, Qc/cVO2 doubled (P = 0.02) and cEo2 tended to decrease (5% absolute, P = 1.0). Regional wet-to-dry brain weight ratios after 72 h of hypoxia were 4-13% greater than their respective ratios during normoxia (0.001 less than P less than or equal to 0.05); indirect evidence suggests that this increased brain water content was extravascular. The sheep may be an appropriate model for the further study of high-altitude cerebral edema.