Role of Prostaglandins in Modulating Sympathetic Vasoconstriction in the Cerebral Circulation in Anesthetized Rabbits

Abstract

The effects of the interaction between sympathetic nerves and prostaglandins in the cerebral circulation were examined. The hypothesis tested was that inhibition of prostaglandin synthesis by indomethacin would potentiate decreases in CBF caused by sympathetic nerve stimulation. In anesthetized rabbits, following administration of either indomethacin (10 mg/kg) or vehicle, CBF was measured with 15-μm microspheres prior to stimulation and following 3–5 min of electrical stimulation (4, 8, 16 Hz) of both superior cervical ganglia. In the vehicle group, CBF was 33–42 ml/min/100 g prior to stimulation. Bilateral sympathetic stimulation reduced blood flow to the cerebrum by 12 ± 6% (mean ± SEM) (p < 0.05) at 4 Hz (n = 8), by 20 ± 4% (p < 0.05) at 8 Hz (n = 12), and 21 ± 6% (p < 0.05) at 16 Hz (n = 11). In the indomethacin group, CBF was 37–48 ml/min/100 g prior to stimulation. Bilateral stimulation decreased blood flow to the cerebrum by 7 ± 5% (NS) at 4 Hz (n = 8), by 25 ± 3% (p < 0.05) at 8 Hz (n = 6), and by 20 ± 6% (NS) at 16 Hz (n = 6). Decreases in CBF during nerve stimulation were blocked by prazosin, an α-adrenergic antagonist. In additional experiments, cerebral vascular constrictor responses to hypocapnia were found to be similar in the vehicle and indomethacin groups. This study provides evidence that sympathetic nerves can decrease CBF substantially even at low stimulation frequencies. Further, results of this study indicate that prostaglandins do not attenuate the effects of sympathetic stimulation on the cerebral circulation.