Effect of the cyclo-oxygenase blocker ibuprofen on cerebral blood volume and cerebral blood flow during normocarbia and hypercarbia in newborn piglets

Indomethacin modifies baseline cerebral haemodynamics and metabolism, as we ll as vasomotor adaptive responses. However, the significance of arachidoni c acid metabolites in the regulation of cerebral circulation remains unclea r. A study was made of the effect of inhibition of the cyclooxygenase pathw ay on baseline cerebral haemodynamics and CO2-induced vasodilation using th e more specific cyclo-oxygenase blocker ibuprofen in a neonatal pig model. Two methods were used: radiolabelled microspheres to measure cerebral blood flow and near infrared spectroscopy to calculate absolute changes in cereb ral blood volume. The relationship between CO2-induced changes in these two haemodynamic parameters was evaluated. Fifteen newborn piglets <7 d old re ceived an i.v. infusion of either ibuprofen (30 mg/kg) (IB group. n = 8) or saline (control group, n = 7). Cerebral blood flow and absolute changes in cerebral blood volume were measured while the piglets were breathing room air at baseline and 30 min after infusion of ibuprofen or saline, and 15 mi n and 30 min after inducing hypercarbia. Global and regional cerebral blood Bow (ml/hg/min) and absolute changes in cerebral blood volume (ml/hg) did not vary between baseline and 30 min after infusion of ibuprofen or saline. During hypercarbia, global and regional cerebral blood Bow and absolute ch anges in cerebral blood volume increased significantly in both the ibuprofe n and control groups (p < 0.01). The mean percentage increases in blood flo w and blood volume at each measurement were almost identical, with approxim ately 90% of the increase in both parameters occurring after 15 min of hype rcarbia, then reaching a plateau. However, we found no agreement between ce rebral blood flow changes and absolute changes in cerebral blood volume. We conclude that ibuprofen did not alter either baseline cerebral circulation or physiological CO2-induced vasodilation in newborn pigs. We speculate th at hypercarbic cerebral vasodilation could be caused either by mediators ot her than the cyclo-oxygenase metabolites of arachidonic acid or by a direct effect on vessel walls.