CEREBRAL PRESSURE-FLOW AND METABOLIC RESPONSES TO SUSTAINED HYPOXIA -EFFECT OF CO2

This study was designed to determine the role of CO2 in the cerebral h emodynamic, metabolic, and fluid shift responses in a conscious sheep model of acute mountain sickness (AMS). Ewes were instrumented chronic ally with left ventricular, aortic, inferior vena cava, sagittal sinus , and epidural catheters and exposed to 96 h of hypoxia in an environm ental chamber in two groups: 1) hypocapnic [HH; n = 12; arterial PO2 ( Pa-O2) = 40 Torr, arterial PCO2 (Pa-CO2) = 27 Torr] and 2) eucapnic (E H; n = 9; Pa-O2 = 40 Torr, Pace, = 37 Torr). AMS, estimated from food and water intakes and behavior, occurred in 9 of 12 HH and 9 of 9 EH s heep. Intracranial pressure (Picp) and the pressure gradient between P icp and sagittal sinus (Psag) increased in AMS sheep only. Total and r egional cerebral blood flows, except in the choroid plexus (Qcp), were elevated significantly (P < 0.05) throughout hypoxia in all sheep; ce rebral blood flow was greater in EH sheep (P < 0.05). Qcp decreased in HH (P < 0.05) but remained unchanged in EH sheep. Cerebral O-2, and g lucose uptakes were not altered in either group. Brain edema, reflecte d by elevated wet-to-dry tissue weight ratios (P < 0.0001), occurred o nly in AMS sheep. We conclude 1) AMS is associated with cerebral edema and normal brain aerobic metabolism, 2) decreased Qcp and increased P icp-Psag gradients during HH likely compensate the increased intracran ial volume in AMS, and 3) CO2 supplementation at constant Pa-O2 did no t reduce AMS, Picp, or brain tissue edema.