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首页> 外文期刊>The Annals of otology, rhinology, and laryngology >Effect of nitric oxide synthase inhibitor on increase in nasal mucosal blood flow induced by sensory and parasympathetic nerve stimulation in rats.
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Effect of nitric oxide synthase inhibitor on increase in nasal mucosal blood flow induced by sensory and parasympathetic nerve stimulation in rats.

机译:一氧化氮合酶抑制剂对感觉和副交感神经刺激引起的鼻粘膜血流量增加的影响。

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OBJECTIVES: Neural control of nasal blood flow (NBF) has not been systematically investigated. The aim of the present study was to evaluate the effect of electrical stimulation of both sensory and parasympathetic nerves innervating the nasal mucosal arteries on NBF in rats. METHODS: In anesthetized rats, nasociliary (sensory) nerves and postganglionic (parasympathetic) nerves derived from the right sphenopalatine ganglion were electrically stimulated. We measured NBF with a laser-Doppler flowmeter. RESULTS: The nerve stimulation increased NBF on both sides and increased the mean arterial blood pressure. The increase in NBF was larger on the ipsilateral side than on the contralateral side. Hexamethonium bromide, a ganglion blocker, abolished the stimulation-induced pressure effect and the increase in NBF on the contralateral side, but did not abolish the increase in NBF on the ipsilateral side. The remaining increase in NBF was abolished by N(G)-nitro-L-arginine, a nitric oxide synthase inhibitor. Histochemical analysis with nicotinamide adenine dinucleotide phosphate-diaphorase showed neuronal nitric oxide synthase-containing nerves that innervate nasal mucosal arteries. CONCLUSIONS: Nitric oxide released from parasympathetic nitrergic nerves may contribute to an increase in NBF in rats. The afferent impulses induced by sensory nerve stimulation may lead to an increase in mean arterial blood pressure that is partly responsible for the increase in NBF.
机译:目的:尚未系统地研究鼻腔血流(NBF)的神经控制。本研究的目的是评估电刺激支配鼻粘膜动脉的感觉神经和副交感神经对NBF的影响。方法:在麻醉大鼠中,电刺激源自右侧蝶神经节的鼻睫(感觉)神经和节后(副交感神经)神经。我们用激光多普勒流量计测量了NBF。结果:神经刺激增加了两侧的NBF,并增加了平均动脉血压。同侧的NBF增幅大于对侧的NBF。神经节阻滞剂溴化六溴铵消除了刺激引起的压力效应和对侧的NBF的增加,但没有消除同侧的NBF的增加。 NBF的剩余增加被一氧化氮合酶抑制剂N(G)-硝基-L-精氨酸消除。用烟酰胺腺嘌呤二核苷酸磷酸-心肌黄酶的组织化学分析显示,含有神经一氧化氮合酶的神经支配着鼻粘膜动脉。结论:副交感神经能神经释放的一氧化氮可能导致大鼠NBF升高。感觉神经刺激引起的传入冲动可能导致平均动脉血压升高,这是造成NBF升高的部分原因。

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