Effects of capsaicin and nitric oxide synthase inhibitor on increase in cerebral blood flow induced by sensory and parasympathetic nerve stimulation in the rat
Effects of capsaicin and nitric oxide synthase inhibitor on increase in cerebral blood flow induced by sensory and parasympathetic nerve stimulation in the rat
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DOI：
10.1152/japplphysiol.00690.2004
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发表时间：
2005-05-01
影响因子：
3.3
通讯作者：
Okamura, T
中科院分区：
文献类型：
--
作者：
Ayajiki, K;Fujioka, H;Okamura, T
用激光多普勒血流仪和血压监测系统研究了电刺激支配大脑动脉的感觉神经和副交感神经束对麻醉大鼠脑血流量（CBF）和平均动脉血压（MABP）的影响。电极钩接在神经束上，包括来自三叉神经的鼻睫远端神经和来自蝶腭神经节的副交感神经纤维。对照组大鼠神经刺激30 s后，同侧CBF和MABP均增加。六甲溴铵降低了CBF的增加，并消除了MABP的CBF增加。在六甲铵处理下，n- g -硝基- l -精氨酸（L-NNA, 1 mg/ kg）显著减弱刺激引起的CBF增加，添加l -精氨酸后CBF恢复。尽管将L-NNA剂量提高到10 mg/ kg，但刺激引起的CBF增加并未进一步抑制，也从未被消除。在辣椒素预处理大鼠中，刺激诱导的CBF和MABP的增加幅度低于对照大鼠。六甲溴铵降低了CBF的增加，并消除了MABP的CBF增加。在六甲铵处理下，L-NNA消除了辣椒素预处理大鼠刺激引起的CBF增加。综上所述，副交感神经释放的一氧化氮和感觉神经释放的神经肽可能是大鼠CBF增加的原因。神经刺激传入冲动可刺激三叉神经，导致MABP快速升高，这是CBF增加的部分原因。
Effects of electrical stimulation of the nerve bundles including sensory and parasympathetic nerves innervating cerebral arteries on cerebral blood flow (CBF) and mean arterial blood pressure ( MABP) were investigated with a laser-Doppler flowmeter and a blood pressure monitoring system in anesthetized rats pretreated with and without capsaicin. The electrode was hooked on the nerve bundles including the distal nasociliary nerve from trigeminal nerve and parasympathetic nerve fibers from sphenopalatine ganglion. In control rats, the nerve stimulation for 30 s increased CBF in the ipsilateral side and MABP. Hexamethonium attenuated the increase in CBF and abolished that in MABP. Under treatment with hexamethonium, N-G-nitro-L-arginine (L-NNA, 1 mg/ kg) significantly attenuated the stimulation-induced increase in CBF, which was restored by the addition of L-arginine. Although the dose of L-NNA was raised up to 10 mg/ kg, the stimulation-induced increase in CBF was not further inhibited and was never abolished. In capsaicin-pretreated rats, magnitudes of the stimulation-induced increases in CBF and MABP were lower than those in control rats. Hexamethonium attenuated the increase in CBF and abolished that in MABP. Under treatment with hexamethonium, L-NNA abolished the stimulation-induced increase in CBF in capsaicin-pretreated rats. In conclusion, nitric oxide released from parasympathetic nerves and neuropeptide( s) released antidromically from sensory nerves may be responsible for the increase in CBF in the rat. The afferent impulses by nerve stimulation may stimulate the trigeminal nerve and lead to the rapid increase in MABP, which partly contributes to the increase in CBF.