The aims of the study were to evaluate the effect of epinephrine-containing local anesthetics on pulpal blood flow (PBF) and to investigate its effect on cavity preparation-induced PBF change. PBF was recorded using a laser Doppler flowmeter (Perimed Co., Sweden) from canines of nine cats under general anesthesia before and after injection of local anesthetics and after cavity preparation. 2% lidocaine hydrochloride with 1 : 100,000 epinephrine was administered by local infiltration given apical to the mandibular canine at the vestibular area and the same volume of isotonic saline was injected on the contralateral tooth as a control. A round carbide bur was operated at slow speed with isotonic saline flushing to grind spherical cavities with increasing depth through the enamel and into the dentin on both teeth. The obtained data was analyzed with paired t-test.

Cavity preparation caused significant increase of PBF (n = 9, p < 0.05). Local infiltration of lidocaine with epinephrine resulted in decreases of PBF (n = 9, p < 0.05), whereas there was no significant change of PBF with the physiologic saline as a control. Cavity preparation on tooth anesthetized with lidocaine with epinephrine caused significantly less increase of PBF than in control tooth (p < 0.05).

Therefore, the result of the present study demonstrates that local infiltration of 2% lidocaine with 1 : 100,000 epinephrine effectively reduces PBF increase caused by cavity preparation.

The purpose of this study was to investigate the function of calcitonin gene-related peptide (CGRP) in regulatory mechanism of pulpal microcirculation with the aim of elucidating neurogenic inflammation.

Experiments were performed on twelve cats under general anesthesia. CGRP was administered through the femoral vein to see the systemic influence and through the external carotid artery to see the local effect. Sympathetic nerve to the dental pulp was stimulated electrically and pulpal blood flow (PBF) was measured with a laser Doppler flowmeter on the canine teeth to the drug administration. The paired variables of control and experimental data were compared by paired t-test and differences with p < 0.05 were considered statistically significant.

Systemic administration of CGRP (0.3 μg/kg) exerted decreases in systemic blood pressure and caused changes in PBF with an initial increase followed by decrease and a more marked second increase and decrease.

Close intra-arterial (i.a.) injection of CGRP (0.03 μ/kg) resulted in slight PBF increase. The effect of CGRP resulted in no significant increase in PBF in the presence of CGRP_8-37.

The electrical stimulation of the sympathetic nerve alone resulted in PBF decreases. The i.a. administration of CGRP following the electrical stimulation of the sympathetic nerve compensated the decreased PBF. Therefore, CGRP effectively blocked the sympathetic nerve stimulation-induced PBF decrease.

Results of the present study have provided evidences that even though the local vasodilatory function of CGRP are weak, CGRP is effectively involved in blocking the vasoconstriction caused by sympathetic nerve stimulation in the feline dental pulp.

The purpose of this study was to investigate the influence of NK1 receptor antagonists on the pulpal blood flow (PBF) when applied iontophoretically through the dentinal cavity of the teeth in order to understand whether iontophoretically applied NK1 receptor antagonists can control the pulpal inflammation.

Eleven cats were anesthetized with alpha-chloralose and urethane, and substance P (SP) was administered to the dental pulp through the catheterized lingual artery in doses that caused PBF change without the influence of systemic blood pressure. NK1 receptor antagonists were applied iontophoretically to the prepared dentinal cavity of ipsilateral canine teeth of the drug administration, and PBF was monitored. Data were analyzed statistically with paired t-test.

PBF increase after iontophoretic application of the NK1 receptor antagonists followed by the intra-arterial administration of SP was significantly less than PBF increase after iontophoretic application of the 0.9% saline followed by the intra-arterial administration of SP as a control (p < 0.05).

Iontophoretic application of the NK1 receptor antagonists (0.2~3.4 mM) following the intra-arterial administration of SP resulted in less increase of PBF than the iontophoretic application of the 0.9% saline following the intra-arterial administration of SP as a control (p < 0.05).

Therefore, the results of the present study provide evidences that the iontophoretic application is an effective method to deliver drugs to the dental pulp, and that iontophoretically applied NK1 receptor antagonists block SP-induced vasodilation effectively. The above results show the possibility that the iontophoretical application of NK1 receptor antagonists can control the neurogenic inflammation in the dental pulp.