An attempt to demonstrate cerebral anoxia during hyperventilation of anesthetized dogs

¹ Physiology Branch, School of Aerospace Medicine, Brooks Air Force Base, Texas

Eight anesthetized, curarized dogs were ventilated to alveolar Pco₂ of 40, 20, and 10 mm Hg. Blood samples were drawn from an artery and sagittal sinus and analyzed for Pco₂, Po₂, pH, hemoglobin saturation, lactic acid, and pyruvic acid. The vasoconstriction of the cerebral vessels was clearly demonstrated by the increased arteriovenous difference in hemoglobin saturation which increased on the average from 26% to 45% and to 48% during the two periods of hyperventilation. Sagittal sinus Po₂ declined from 41 mm Hg during the control to 29 and to 25 mm Hg with hyperventilation. Calculation of the cerebral "excess lactate" production from the measurements of lactic and pyruvic acids showed no significant increase with hyperventilation. The conclusion was made, with reservation, that cerebral oxygenation during even severe hyperventilation was sufficient to maintain normal oxidative metabolism.