Ishii Hisayoshi, Sato Toshiya, Izumi Hiroshi
Division of Physiology, Department of Oral Biology, School of Dentistry, Health Sciences University of Hokkaido, 1757 Kanazawa, Ishikari-Tobetsu, Hokkaido, 061-0293, Japan,
J Comp Physiol B. 2014 Apr;184(3):385-99. doi: 10.1007/s00360-014-0807-2. Epub 2014 Feb 7.
We investigated the role of parasympathetic reflex vasodilation in the regulation of the cerebral hemodynamics, and whether GABAA receptors modulate the response. We examined the effects of activation of the parasympathetic fibers through trigeminal afferent inputs on blood flow in the internal carotid artery (ICABF) and the cerebral blood vessels (rCBF) in parietal cortex in urethane-anesthetized rats. Electrical stimulation of the central cut end of the lingual nerve (LN) elicited intensity- and frequency-dependent increases in ICABF that were independent of changes in external carotid artery blood flow. Increases in ICABF were elicited by LN stimulation regardless of the presence or absence of sympathetic innervation. The ICABF increases evoked by LN stimulation were almost abolished by the intravenous administration of hexamethonium (10 mg kg(-1)) and were reduced significantly by atropine administration (0.1 mg kg(-1)). Although the LN stimulation alone had no significant effect on rCBF, LN stimulation in combination with a blocker of the GABAA receptor pentylenetetrazole increased the rCBF markedly. This increase in rCBF was reduced significantly by the administration of hexamethonium and atropine. These observations indicate that the increases in both ICABF and rCBF are evoked by parasympathetic activation via the trigeminal-mediated reflex. The rCBF increase evoked by LN stimulation is thought to be limited by the GABAA receptors in the central nervous system. These results suggest that the parasympathetic reflex vasodilation and its modulation mediated by GABA receptors within synaptic transmission in the brainstem are involved in the regulation of the cerebral hemodynamics during trigeminal afferent inputs.
我们研究了副交感神经反射性血管舒张在脑血流动力学调节中的作用，以及γ-氨基丁酸A型（GABAA）受体是否调节该反应。我们检测了通过三叉神经传入输入激活副交感神经纤维对乌拉坦麻醉大鼠颈内动脉血流量（ICABF）和顶叶皮质脑血管血流量（rCBF）的影响。电刺激舌神经（LN）的中枢切断端可引起ICABF强度和频率依赖性增加，且与颈外动脉血流量变化无关。无论有无交感神经支配，LN刺激均可引起ICABF增加。静脉注射六甲铵（10 mg·kg-1）几乎可消除LN刺激引起的ICABF增加，而阿托品（0.1 mg·kg-1）给药可使其显著降低。虽然单独的LN刺激对rCBF无显著影响，但LN刺激联合GABAA受体阻滞剂戊四氮可显著增加rCBF。六甲铵和阿托品给药可显著降低rCBF的这种增加。这些观察结果表明，ICABF和rCBF的增加均由通过三叉神经介导的反射激活副交感神经引起。LN刺激引起的rCBF增加被认为受中枢神经系统中GABAA受体的限制。这些结果表明，在三叉神经传入输入期间，脑干突触传递中由GABA受体介导的副交感神经反射性血管舒张及其调节参与了脑血流动力学的调节。
