THE INFLUENCE OF THE TRIGEMINAL GANGLION ON CAROTID BLOOD-FLOW IN ANESTHETIZED GUINEA-PIGS

1 The influence of the trigeminal ganglion on the carotid circulation has been investigated by measuring electrical stimulation-induced alte rations in carotid arterial blood flow and resistance in anaesthetized guinea-pigs. The effects of several receptor antagonists were assesse d to determine which neurotransmitters are involved in regulating caro tid blood flow. 2 Arterial blood pressure and carotid vascular resista nce were reduced by electrical stimulation (0.5 mA, 1 ms, 5 Hz, 60 s) of the trigeminal ganglion ipsilateral to the carotid artery from whic h flow was measured. No consistent effect of electrical stimulation on carotid blood flow was observed. However, when guinea-pigs were pretr eated with guanethidine (30 mg kg(-1), s.c., 24h prior to experiments) , stimulation produced little change in blood pressure, while carotid blood flow was increased and vascular resistance decreased, consistent with vasodilatation in the cranial circulation. Stimulation of the tr igeminal ganglion contralateral to the carotid artery from which blood flow was measured, had little effect on either carotid blood flow or vascular resistance. 3 In animals pretreated with guanethidine, intrav enous administration of the vasoactive intestinal polypeptide (VIP) re ceptor antagonist, p-Cl-D-Phe(6),Leu(17)-VIP (50 mu g kg(-1)) signif icantly attenuated the increase in carotid blood flow and decrease in carotid vascular resistance evoked by trigeminal ganglion stimulation. Responses evoked by trigeminal ganglion stimulation were, however, un affected by intravenous injection of the tachykinin NK1 receptor antag onists, GR82334 (0.3 mg kg(-1)) and CP-99,994 (0.4 mg kg(-1)), calcito nin gene-related peptide (CGRP) receptor antagonist, CGRP(8-37) (0.9 m g kg(-1)) and the ganglion blocking agent, hexamethonium (10 mg kg(-1) ). 4 It is concluded that in the guanethidine-pretreated guinea-pig, e lectrical stimulation of the trigeminal ganglion increases carotid blo od flow and produces an accompanying decrease in carotid vascular resi stance; consistent with the dilatation of carotid blood vessels. The t ransmitter mediating this effect is most likely to be VIP.