Cerebral oxygen consumption and blood flow in hypoxia: influence of sympathoadrenal activation.

Abstract

The effect of hypoxia (reduction of arterial PO2 [partial pressure of O2] to 26-28 mm Hg) on cerebral blood flow (CBF) and cerebral O2 consumption (CMRO2) was studied in paralyzed and artificially ventilated rats using a CBF technique of improved accuracy at high flow rates. Animals maintained on 70% N2O unexpectedly showed that hypoxia of this severity is accompanied by an increase in CMRO2; 2 different mechanisms apparently are involved, both related to catecholamine metabolism. In 1 breed of Wistar rats hypoxia was accompanied by a 6-fold increase in CBF and by an increase in CMRO2 to 180% of control. Prior removal of the adrenal glands curtailed the increase in CBF (400% of control) and CMRO2 (125% of control). The excessive increase in CMRO2 (to 180% of control) did not occur in another breed of Wistar rats. Since infusion of adrenaline [epinephrine] in normoxic animals gave rise to a doubling of CMRO2, under some circumstances circulating catecholamines can apparently increase O2 consumption in the hypoxic brain. In the 2nd breed of rats hypoxia was consistently accompanied by a 20-30% increase in CMRO2 which was unaffected by prior adrenalectomy. Since the increase was prevented by sedative and anesthetic doses of diazepam, the increase was probably elicited by increased activity in cerebral catecholaminergic pathways. The conclusion is supported by parallel studies showing that a similar increase in CMRO2 occurs in hypercapnia which is blocked by diazepam and propranolol.