Effect of indomethacin on basal and carbon dioxide stimulated cerebral blood flow in man

Abstract

Summary. Cerebral blood flow (CBF) was measured using the nitrous oxide technique in the basal state and following inhalation of CO2 in eight, healthy, awake male volunteers, before and during inhibition of prostaglandin synthesis with indomethacin. Arterial and jugular venous oxygen contents and pCO2 were also analysed. Indomethacin reduced the basal CBF by 35%, from 43 ± 2 to 28 ± 2 ml/100 ml tissue per min, but did not affect the calculated cerebral metabolic rate of oxygen (CMRO2). The reduced CBF was accompanied by an elevation of jugular venous pCO2. Inhalation of 6–7% CO2 increased CBF to 98 ± 17 ml/100 ml tissue per min before indomethacin, compared with only 42 ± 4 ml/100 ml tissue per min after indomethacin. This difference in the hypercapnia induced increase in CBF before and after indomethacin was reflected also by the data on arterio‐venous differences in pCO2.We conclude that indomethacin inhibits both basal and hypercapnia stimulated CBF in man and suggest that this effect of the drug is due to inhibition of prostaglandin formation. If so, cerebral vascular PG formation plays an important role not only in the maintenance of CBF during normocapnia, but also in the cerebral vasodilation associated with elevated arterial pCO2.