Division of Physiology, Department of Oral Biology, School of Dentistry, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido 061-0293, Japan.
Brain Res. 2010 Feb 2;1312:41-53. doi: 10.1016/j.brainres.2009.11.073. Epub 2009 Dec 5.
The present study examined whether vagal visceral inputs are involved in parasympathetic reflex vasodilatation in the masseter muscle in urethane-anesthetized and cervically sympathectomized rats. Electrical stimulation of the central cut end of the cervical vagus nerve (VN) including visceral afferent fibers, which consisted of cervical/thoracic branches (heart and lungs) and abdominal branches (entire gastrointestinal tract), elicited intensity- and frequency-dependent increases of blood flow in the masseter muscle (MBF). Activation of the abdominal VN inferior to the diaphragm failed to affect the MBF. MBF increases evoked by cervical VN stimulation were reduced significantly by hexamethonium. Pretreatment with atropine reduced the MBF increase evoked by VN stimulation significantly, whereas pretreatment with either propranolol or phentolamine had no effect on the response. MBF increases occurred with electrical stimulation of nucleus of the solitary tract (NTS), and these increases were significantly reduced by the administration of hexamethonium and atropine. MBF increases also occurred after microinjection of glutamate into the NTS in a dose-dependent manner. Microinjection of muscimol into the NTS caused a significant attenuation of the VN stimulation-induced MBF increases. Our results suggest that vagal visceral inputs passing to the NTS are involved in the parasympathetic reflex vasodilatation in the rat masseter muscle. The MBF increase evoked by the vagal-parasympathetic reflex mechanism occurred via visceral afferents running in the cervical VN, but not in the abdominal VN, suggesting that the vagal visceral afferents derived from cardiovascular and/or respiratory systems may play an important role in the regulation of the MBF.
本研究旨在探讨迷走内脏传入在颈交感神经切断和氨基甲酸乙酯麻醉大鼠咀嚼肌副交感反射性血管舒张中的作用。电刺激颈迷走神经中央端（包括颈/胸支（心脏和肺）和腹支（整个胃肠道）的内脏传入纤维），可引起咀嚼肌血流（MBF）的强度和频率依赖性增加。膈下的腹迷走神经的激活不能影响 MBF。颈迷走神经刺激引起的 MBF 增加明显被六烃季铵减少。预先用阿托品处理可显著减少 VN 刺激引起的 MBF 增加，而预先用普萘洛尔或酚妥拉明处理对反应无影响。电刺激孤束核（NTS）可引起 MBF 增加，给予六烃季铵和阿托品可显著减少这种增加。谷氨酸微注射到 NTS 也可引起 MBF 呈剂量依赖性增加。微注射到 NTS 的 muscimol 可显著减弱 VN 刺激引起的 MBF 增加。我们的结果表明，传入 NTS 的迷走内脏传入参与了大鼠咀嚼肌的副交感反射性血管舒张。迷走神经-副交感反射机制引起的 MBF 增加是通过在颈迷走神经中运行的内脏传入纤维引起的，但在腹迷走神经中没有，这表明来自心血管和/或呼吸系统的迷走内脏传入可能在调节 MBF 中发挥重要作用。
