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The regulatory mechanism of the pulpal microcirculatory hemodynamics was investigated by measuring pulpal blood flow (PBF) in dogs by means of a laser doppler flowmeter. Application of vasodilators (acetylcholine, isoproterenol, histamine, bradykinin and substance P) to the prepared cavity caused an increase in PBF, and norepinephrine reduced PBF. These vasoactive substance-induced responses, but not the bradykinin-induced response, were inhibited by i.v. injection of antagonists (atropine, propranolol, diphenhydramine and [D-Pro2, D-Trp7,9]-substance P). The effect of bradykinin was inhibited by indomethacin, but not by des-Arg9-[Leu8]-bradykinin. Furthermore, prostaglandin E2 produced a concentration-dependent increase in PBF. These results suggest that acetylcholine, histamine, bradykinin, substance P and norepinephrine, if present, influence the local vasomotor regulation in the dental pulp, and that bradykinin may exert the effect via prostaglandin synthesis. Based on this suggestion, the effect of electrical stimulation of the distal end of the cut inferior alveolar nerve on PBF was studied. The nerve stimulation-induced increase in PBF was inhibited by indomethacin, but not by atropine, propranolol, diphenhydramine, soybean trypsin inhibitor, aprotinin, des-Arg9-[Leu8]-bradykinin, or by [D-Pro2, D-Trp7,9]-substance P. The experiments show that the increase in PBF produced by stimulation of the inferior alveolar nerve is not mediated by common efferent vasodilatory mechanisms, and it is probably mediated by prostaglandin release via the sensory nerve axon reflex mechanism.

Effect of vasoactive substances and electrical stimulation of the inferior alveolar nerve on blood flow in the dental pulp in dogs.