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Abstract

Cerebrovascular regulation during perturbations in arterial CO₂ is thought to occur solely at the level of the pial vessels. However, recent evidence implicates large extra-cranial cerebral blood vessels in this regulatory process. Although the mechanisms governing CO₂ mediated vasomotion remain unclear, animal and human studies support a large role of prostaglandins. Thus, we examined two hypotheses: 1) vasomotion of the internal carotid artery (ICA) would occur in response to both hyper and hypocapnia; and 2) pharmacological inhibition of prostaglandin synthesis with Indomethacin (INDO; a non-selective cyclooxygenase inhibitor) would reduce the vasomotor response of the ICA to changes in end-tidal PCO₂ (PETCO₂). Using a randomized single-blind placebo controlled study, subjects (n=10) were tested on two occasions. Before and 90-minutes following either oral INDO (1.2mg/kg) or placebo capsule, concurrent measures of beat-by-beat blood flow, velocity and diameter of the ICA were made at rest and during steady state stages (4 min) of iso-oxic hypercapnia (+3, +6, +9mmHg above baseline) and hypocapnia (-3, -6, -9mmHg below baseline). End-tidal forcing was employed for the control of blood gases. To examine if INDO affected ICA vasomotion in a cyclooxygenase inhibition independent manner, a subset of subjects (n=5) were tested before and 45-minutes following oral Ketorolac (0.25mg/kg). During pre-drug testing in the INDO trial, the ICA dilated during hypercapnia at +6mmHg (4.72±0.45 vs. 4.95±0.51mm; P