Cerebral Blood Flow and Oxygen Consumption in the Rat Brain during Extreme Hypercarbia

Abstract

The effects of hypercapnia (PaCO2 80, 160 and 300 torr) on cerebral metabolic rate for O2 (CMRO2) and blood flow (CBF) were evaluated in paralyzed, mechanically ventilated rats by a 133Xe modification of the Kety-Schmidt inert-gas technique. Hypercapnic rats (PaCO2 80 torr) maintained on 70% N2O, had a 6-fold increase in CBF and a 25% increase in CMRO2, which were not prevented by adrenalectomy or decreases in tissue O2 tensions to near-normal values. Further increases in arterial blood CO2 tensions were associated with decreases in CMRO2 to normal (PaCO2 160 torr) or subnormal values (PaCO2 300 torr). In the latter case there was only a 3-fold increase in CBF. In rats with PacO2 .apprx. 80 torr that were given 2.5 mg/kg 2.5 propranolol during N2O anesthesia, there was only a 3-fold increase in CBF, while CMRO2 decreased to below normocapnic control values. Rats with PaCO2 80 torr given sedative or anesthetic doses of diazepam (ventilated with 30% O2 in N2) also had decreased CMRO2 values and had a 2-fold increase in CBF. Hypercapnia apparently activates adrenergic receptors in the brain, and this activation increases O2 consumption. The increase in flow that occurs with hypercapnia is markedly influenced by activity in adrenergic neurons.