• J D Pickard, J E Rose, M D Shaw, and A Strathdee.
• Br. J. Pharmacol. 1980 Mar 1; 68 (3): 407-11.

Abstract1 The effect of intravenous sodium salicylate on cerebral oxygen consumption and cerebral blood flow and its response to hypercapnia was measured by the 133Xenon intracarotid injection technique in ten baboons. 2 After an initial peak, the plasma salicylate level maintained a stable value for 2 h of 1 mmol/l with 50 mg/kg sodium salicylate and 2.5 mmol/l with 200 mg/kg sodium salicylate. 3 Sodium salicylate (50 mg/kg) produced no change in baseline cerebral blood flow (CBF) or cerebral oxygen consumption (CMRO2) but the CBF response to hypercapnia was reduced by 41% during the first hour. During the second hour after salicylate administration, CMRO2 increased by 26%, CBF at normocapnia increased by 31% and the CBF response to hypercapnia was 67% of the baseline value. 4 Sodium salicylate (200 mg/kg) increased CMRO2 by 65%. There was no significant change in CBF at normocapnia or hypercapnia. 5 These results confirm that inhibitors of prostaglandin synthesis, which can cross the blood brain barrier in sufficient quantity, reduce the response of the cerebral circulation to hypercapnia. The difficulties in interpreting changes in the CBF CO2 response in the presence of increases in CMRO2 are discussed. It is suggested that the respiratory stimulation seen in salicylate intoxication is the result of a central metabolic stimulation.

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