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咀嚼肌的副交感反射性血管扩张可补偿迷走神经介导的降压反应期间颈动脉灌注不足。

Parasympathetic reflex vasodilatation in the masseter muscle compensates for carotid hypoperfusion during the vagus-mediated depressor response.

机构信息

Division of Physiology, Department of Oral Biology, School of Dentistry, Health Sciences University of Hokkaido, Ishikari-Tobetsu, Hokkaido, Japan.

出版信息

Brain Res. 2011 Jan 25;1370:145-53. doi: 10.1016/j.brainres.2010.11.046. Epub 2010 Nov 17.

DOI:10.1016/j.brainres.2010.11.046
PMID:21093419
Abstract

Parasympathetic vasodilatation in the orofacial area is thought to be an important factor in the regulation of blood flow in the common carotid artery (CABF), and disturbances in parasympathetic vasodilatations may be related to impairment of the CABF inducing craniofacial ischemia. We hypothesized that the parasympathetic vasodilatation in the masseter muscle evoked by a vagus-mediated reflex is involved in the maintenance of the CABF during the vagus-mediated depressor response. In the present study, we compared changes in blood flow in the masseter muscle (MBF) and CABF, and systemic arterial blood pressure (SABP) evoked by electrical stimulation of the central cut end of the cervical vagus nerve (cVN) in anesthetized and sympathectomized rats. Electrical stimulation of the cVN in the sympathectomized animals caused an increase in MBF followed by a CABF increase, although it simultaneously induced a decrease in SABP. These increases in blood flow changed to decreases after intravenous administration of atropine (100 μg/kg), while pretreatment with atropine had no effect on the changes in SABP. Microinjection (50 nl/site) of the muscimol (1mM), into the nucleus of the solitary tract, which is involved in reflex cardiovascular regulation, markedly inhibited the cVN stimulation-induced MBF increase. Our results indicate that vagal-parasympathetic vasodilatation in the masseter muscle compensates for carotid hypoperfusion during the vagus-mediated depressor response, and that GABAergic neurons may be involved in the inhibition of this response. This inhibition may result in the impairment of CABF, suggesting an important role in the etiology of neurally mediated syncope.

摘要

咀嚼肌的副交感神经血管舒张被认为是调节颈总动脉血流的一个重要因素,副交感神经血管舒张功能障碍可能与颈总动脉血流减少引起的颅面缺血有关。我们假设迷走神经介导的降压反应中,由迷走神经介导的反射引起的咀嚼肌副交感神经血管舒张参与了颈总动脉血流的维持。在本研究中,我们比较了麻醉和去交感神经大鼠颈迷走神经中枢端电刺激时咀嚼肌血流(MBF)和颈总动脉血流(CABF)以及系统动脉血压(SABP)的变化。在去交感神经大鼠中,cVN 电刺激引起 MBF 增加,随后 CABF 增加,尽管它同时引起 SABP 降低。这些血流变化在静脉注射阿托品(100μg/kg)后变为减少,而预先给予阿托品对 SABP 的变化没有影响。将 1mM 毒蕈碱(muscimol)微注射(50 nl/site)到涉及反射心血管调节的孤束核中,显著抑制了 cVN 刺激引起的 MBF 增加。我们的结果表明,咀嚼肌的迷走副交感神经血管舒张在迷走神经介导的降压反应中补偿了颈动脉灌注不足,而 GABA 能神经元可能参与了这种反应的抑制。这种抑制可能导致 CABF 受损,提示其在神经介导性晕厥的发病机制中起重要作用。

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