Cerebral metabolic and pressure-flow responses during sustained hypoxia in awake sheep.
Conscious sheep (n = 6), exposed to 3.5 h of normobaric hypoxia (arterial PO2 = 40 Torr) while allowed varying arterial PCO2, showed striking early increments of cerebral blood flow (CBF; +200-250%, by radiolabeled microspheres) and decrements of cerebral vascular resistance (CVR) in association with an early temporary elevation of cerebral O2 consumption (CMRO2; +25-60%). After 2 h, CMRO2 returned to normoxic levels, while CBF declined to a lower but still elevated level (+150%). CBF/CMRO2 increased twofold, while cerebral fractional extraction of O2 was unchanged. Mean arterial pressure was unchanged, but cerebral venous pressure rose (+11 mmHg) in a stable fashion such that cerebral perfusion pressure declined by 13%. Cerebral venous hematocrit and hemoglobin concentration were both elevated (+2.2-2.7% Hct units; +1.0-1.3 g/dl, respectively) above the corresponding arterial values between 150 and 210 min of hypoxia, suggesting venous hemoconcentration in possible association with a transcapillary fluid shift. CBF, and especially CVR, were well correlated with arterial O2 content.
Iwamoto
J
J
Department of Physiology, School of Medicine and Biomedical Sciences, State University of New York, Buffalo 14214.
Curran-Everett
D C
DC
Krasney
E
E
Krasney
J A
JA
D000136:Acid-Base Equilibrium / Q000502:physiology; D000818:Animals; D001784:Blood Gas Analysis; D001794:Blood Pressure / Q000502:physiology; D001923:Brain Chemistry / Q000502:physiology*; D001929:Brain Edema / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D005260:Female; D006400:Hematocrit; D006454:Hemoglobins / Q000502:physiology; D006863:Hydrogen-Ion Concentration; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology*; D007427:Intracranial Pressure / Q000502:physiology; D008863:Microspheres; D010101:Oxygen Consumption / Q000502:physiology; D012756:Sheep; D014655:Vascular Resistance / Q000502:physiology
D006454:Hemoglobins