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Antidromic stimulation of sensory nerves has been shown to increase blood flow in the tissue they innervate. This study was designed to determine if antidromic vasomotor responses occur in feline dental pulp and if they are mediated by branched axons supplying both tooth pulp and gingiva. Dynamic changes in pulpal blood flow (PBF) elicited by electrical stimulation, pinching, heating, and capsaicin application to the gingivae were investigated in cat mandibular canine teeth by means of Laser Doppler Velocimetry. All inferior alveolar nerve bundles and the cervical sympathetic trunk had been previously sectioned to avoid the occurrence of brainstem reflexes, e.g., somato-autonomic vasomotor reflexes. Increases in PBF were observed in seven out of 12 cats when a restricted gingival area adjacent to the canine teeth was stimulated as described, but the increases were abolished after the sensitive gingival area was painted with lidocaine jelly, a surface anesthetic. These vasodilator responses, remarkably reduced following repeated application of 30 mM of capsaicin, are considered to be induced via antidromic activation of capsaicin-sensitive nociceptive nerve fibers, presumably by axon reflex mechanisms, suggesting that nerve terminals supplying the gingiva originate from parent axons which have collaterals that innervate the canine tooth pulp.

The purpose of the present study was to investigate the nervous control of gingival blood flow in cats. Gingival blood flow was measured by laser Doppler flowmeter in 75 cats during electrical stimulation and cutting or ligation of the inferior alveolar nerve and cervical sympathetic nerve without sympathectomy or pretreatment with adrenoceptor blocking agents. Three different patterns of responses in gingival blood flow were observed following electrical stimulation of the inferior alveolar nerve in cats. In 45 cats there was an increase in blood flow, in 4 cats a decrease in blood flow, and in 7 cats a biphasic change consisting of an initial decrease and a successive increase in blood flow. The vasodilator effect was significantly reduced by pretreatment with (D-Pro2, D-Trp7.9)-substance P. tripelennamine, and methysergide. Pretreatment with cimetidine, atropine, hexamethonium, phentolamine, or propranolol had no effect on vasodilatation. The vasoconstrictor response was completely inhibited by pretreatment with phentolamine; in this case the vasodilator response appeared after stimulation of the inferior alveolar nerve. Ligation or cutting of the inferior alveolar nerve always elicited an increase in gingival blood flow. Cutting the cervical sympathetic nerve had no effect on gingival blood flow in 8 of 10 cats and caused an increase in gingival blood flow in 2 cats; however, electrical stimulation of the cervical sympathetic nerve always caused a decrease in gingival blood flow in the cats investigated. The present results suggest that cat gingival blood flow is controlled by sympathetic alpha-adrenergic fibers for vasoconstriction and by sensory fibers and mast cells for vasodilatation.

Dynamic changes of pulpal blood flow (PBF) and gingival blood flow (GBF) induced by intra-venous injection of two kinds of vasoactive drugs were observed in dogs by means of Laser Doppler Velocimetry. Intra-venous injection of norepinephrine caused PBF to increase, corresponding to the blood pressure (BP) increase, while GBF decreased. Orciprenaline sulfate caused PBF to decrease parallel to the BP decrease, as compared with a GBF increase. The effects of these vasoactive drugs lasted longer on GBF than on PBF and BP. These results indicate that the regulation of blood flow in the dental pulp is more dependent on systemic blood pressure than on local vasoconstriction or vasodilation.