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Abstracts
In the intact rats, decreased changes in MBF were observed during the MLS, and then after the MLS offset, increased changes in MBF were observed. Any changes in blood pressure were not observed accompanying the MLS. In the experimental group under the sciatic nerve cut, the increased changes in MBF after the MLS offset were abolished, while the decreased changes in MBF during the MHS remained. The time-course changes in MBF accompanying the MLS were not affected by the spinalization. The decreased changes in MBF were abolished under the presence of alpha-adrenergic blocker (phentramine, i.v.), while the increased changes in MBF were abolished under the presence of calcitonin gene-related peptide (CGRP) blocker (hCGRP8-37). These results in the present study suggests; (1) MLS is able to affect a local MBF without evoking any changes in systemic hemodynamics, (2) MLS evokes decreased changes in MBF via alpha-adrenergic receptors without evoking the action of central neural pathway, and (3) MLS induces increased changes in MBF after the stimulation by evoking the action of the axon reflex-like mechanism. doi:10.1016/j.autneu.2007.06.129
I-P-016 Absence of reflex somato-parasympathetic vasodilatation in human dental pulp
changes in pulpal blood flow (PBF) of the maxillary right central incisor and gingival blood flow (GBF) nearby maxillary right central incisor were simultaneously monitored. PBF and GBF responses were evaluated following painful electrical stimulation to the maxillary and mandibular lateral incisors on both side, and topical application of capsaicin to the tongue. PBF and GBF were monitored by means of newly developed transmitted laser light (SNF 12008, Ciberfirm, Japan) and conventional laser Doppler flowmetry (SNF 12007, Ciberfirm, Japan), respectively. Electrical stimulation was performed using electrical pulp tester (Analytic Technology, Pulp Tester, U.S.A.). Results Painful electrical stimulation to the maxillary lateral incisors caused ipsilateral PBF (maxillary central incisor) increases without blood pressure change. However, no PBF change was evoked by painful stimulation of mandibular tooth pulp, or capsaicin application to the tongue, in spite of severe painful sensation. On the other hand, GBF increases were elicited both by painful stimulation of maxillary and mandibular tooth pulp, and capsaicin application to the tongue, on the ipsilateral side. Contralateral painful stimulation to either maxillary or mandibular tooth had no effect on PBF or GBF. Conclusion
Shizuko Satoh-Kuriwada, Takashi Sasano, Astuhiko Mori Division of Oral Diagnosis, Department of Oral Medicine and Surgery, Tohoku University Graduate School of Dentistry, Sendai, Japan Introduction The neural regulation of blood flow in tooth pulp has been demonstrated that there is: (1) sympathetic adrenergic vasoconstriction; (2) alpha-adrenergic vasodilatation; (3) sympathetic cholinergic vasoactive system; and (4) antidromic vasodilator mechanisms involving the sensory nerves, including axon reflex vasodilatation. However, it is yet to be conclusively established whether reflex parasympathetic vasodilatation occurs in the dental pulp, although there have been numerous reports of the existence of reflex parasympathetic vasodilatation in the submandibular gland, nasal mucosa, tongue, lip, and gingiva in various species. This study was designed to determine whether reflex parasympathetic vasodilator mechanisms do or do not exist in the human dental pulp. Subjects and methods 22 healthy volunteers were participated in this experiment whose ages ranged from 19 to 27. An informed consent was obtained from each volunteer. Continuous
These results suggest that axon reflex vasodilator mechanisms might exist, however, somato-parasympathetic vasodilator reflex mechanisms would be absent in human tooth pulp, while both mechanisms exist in human gingiva. These findings are consistent with our previous reports on the tooth-pulp vasomotor responses in the cat (Sasano et al., 1995). doi:10.1016/j.autneu.2007.06.130
I-P-017 Induction of c-Fos expression in the brain of the animal model of posttraumatic stress disorder (PTSD) Kazuyoshi Otake Section of Clinical Anatomy, Tokyo Medical and Dental University, Tokyo, Japan Animals using a single prolonged stress (SPS) paradigm (a number of different stressors in one prolonged session followed by a 1-week ‘no stress’ interval) show enhanced glucocorticoid negative feedback, which is PTSD-specific neuroendocrine abnormality, and are suggested to be an animal model of PTSD. To elucidate the neuronal mechanisms implicated in this negative feedback, we compared