Physiologic effects of hyperventilation and phlebotomy in baboons: systemic and cerebral oxygen extraction.

Eighteen anesthetized baboons were studied to determine the effects of passive hyperventilation and phlebotomy on oxygen transport. After 1 hour of hyperventilation a significant increase in the red cell affinity for oxygen occurred in vivo. This was not associated with any significant changes in cardiac output, oxygen consumption, or in lactic acid production. There was a 40% decrease in cerebral blood flow, a 10 mm Hg decrease in the pulmonary artery Po2 level, and a 17 mm Hg decrease in the jugular venous Po2 level. After 1 hour of hyperventilation, the plasma inorganic phosphorus level decreased significantly, the red cell ATP level decreased slightly, and the red cell 2. 3 DPG level increased significantly, indicating that inorganic phosphorus had been removed from the blood during hyperventilation. Passive hyperventilation was maintained, and the baboons were bled 32% of their red cell volume. The blood volume was partially restored with nonbuffered isotonic saline. One hour after the phlebotomy and volume restoration (2 hours of hyperventilation) there were no changes in oxygen consumption, cardiac output, cerebral blood flow, or blood lactate levels, but the pulmonary artery Po2 level was decreased by 15 mm Hg, and the jugular venous Po2 level was decreased by 20 mm Hg. Systemic oxygen consumption was not affected by the significant decrease in pulmonary artery Po2.