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THE EFFECT OF SODIUM SALICYLATE ON CEREBRAL BLOOD FLOW AND METABOLISM
Author(s) -
PICKARD J.D.,
ROSE J.E.,
SHAW M.D.M.,
STRATHDEE ANN
Publication year - 1980
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1980.tb14554.x
Subject(s) - normocapnia , hypercapnia , cerebral blood flow , sodium salicylate , anesthesia , chemistry , medicine , endocrinology , acidosis
1 The effect of intravenous sodium salicylate on cerebral oxygen consumption and cerebral blood flow and its response to hypercapnia was measured by the 133 Xenon 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 (CMRO 2 ) but the CBF response to hypercapnia was reduced by 41% during the first hour. During the second hour after salicylate administration, CMRO 2 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 CMRO 2 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 CO 2 response in the presence of increases in CMRO 2 are discussed. It is suggested that the respiratory stimulation seen in salicylate intoxication is the result of a central metabolic stimulation.