Cerebral Oxygen Consumption and Blood Flow in Hypoxia: Influence of Sympathoadrenal Activation

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Abstract

SUMMARY

The effect of hypoxia (reduction of arterial Po2 to 26-28 mm Hg) on cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2) was studied in paralyzed and artificially ventilated rats, using a CBF technique of improved accuracy at high flow rates. Results obtained on animals maintained on 70% N2O unexpectedly showed that hypoxia of this severity is accompanied by an increase in CMRO2, and they indicated that 2 different mechanisms are involved, both related to catecholamine metabolism. In one breed of Wistar rats studied, 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. However, since infusion of adrenaline in normoxic animals gave rise to a doubling of CMRO2 it is concluded that, at least under some circumstances, circulating catecholamines can increase oxygen consumption in the hypoxic brain. In the second breed of rats studied, 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, it is tentatively concluded that the increase was elicited by increased activity in cerebral catecholaminergic pathways. The conclusion is supported by parallel studies showing that a similar increase in CMR02 occurs in hypercapnia, which is blocked both by diazepam and propranolol.

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