Microcirculation of the dental pulp and its autonomic control

Pulpal vessels are innervated with sympathetic adrenergic vasoconstrictor fibers. Electrical stimulation of the cervical sympathetic nerve causes pulpal arteriolar constriction and a reduction of arteriolar and venular flow rate (in mm3/s) in rat incisor pulps and a decrease in pulpal blood flow (in ml/min/100 g) in canine pulps of cats and dogs. The alpha-antagonist phenoxybenzamine and the alpha-1 antagonist prazosin attenuated the decrease in pulpal blood flow (PBF) caused by sympathetic stimulation. Reflex excitation of the sympathetic nerve system by hemorrhage caused pulpal vasoconstriction and a reduction of PBF. Induction of hemorrhagic hypotension in dogs subjected to cervical sympathectomy and adrenalectomy caused less pronounced pulpal vasoconstriction and flow reduction than in normal dogs. Pulpal vessels are also equipped with alpha-1, alpha-2 and beta-adrenergic receptors. Activation of alpha-1 and alpha-2 receptors by intraarterial injection of phenylephrine and clonidine caused a reduction in PBF in dogs and decreases in arteriolar and venular diameters and volumetric flow in rats. These responses were blocked by the alpha-1 and alpha-2 antagonists. Activation of beta-2 receptors by i.a. injection of isoproterenol caused a paradoxical reduction of PBF in dogs. In rats isoproterenol caused a transient increase in the flow rate followed by a reduction, and arteriolar dilation was accompanied by venular constriction. These flow responses to isoproterenol were blocked by the beta-2 antagonist propranolol. Results of microcirculatory studies in dogs and rats indicate that pulpal hemodynamics are regulated significantly by the sympathetic adrenergic system.