Watanabe H, Tsuru H, Yajin K, Kawamoto H, Sasa M
Department of Otorhinolaryngology, Hiroshima University School of Medicine, Japan.
Jpn J Pharmacol. 1998 Aug;77(4):287-92. doi: 10.1254/jjp.77.287.
We have previously reported that there is non-adrenergic, non-cholinergic (NANC) innervation in canine nasal mucosa and that the relaxation response to electrical stimulation of the NANC nerve is mainly mediated by nitric oxide (NO). In the present study, we examined the effect of cold exposure (24 degrees C) on nitroxidergic nerve-mediated vasodilatation in isolated canine nasal mucosa. Nasal mucosa strips, prepared from canine nasal septum and moderately precontracted with methoxamine in the presence of atropine and guanethidine, relaxed in response to transmural electrical stimulation (square pulses of 0.5-msec duration, at 5 Hz and 25 V). The degree of relaxation at 24 degrees C (55.4+/-13.2% of methoxamine-induced contraction, mean+/-S.D., n=6) was significantly greater than that at 34 degrees C (33.8+/-8.6%, n=6). This phenomenon was reversible. In contrast, the magnitude of relaxation responses to an NO donor (sodium nitroprusside of 0.1 and 1 microM) remained unchanged by cold exposure. These results suggest that the release of NO from the nitroxidergic nerve endings is augmented by cold exposure and, thus, vasodilatation of the nasal blood vessel is enhanced, thereby contributing to the swelling of the nasal mucosa in cold conditions.
我们之前曾报道，犬鼻黏膜存在非肾上腺素能、非胆碱能（NANC）神经支配，且对NANC神经进行电刺激所产生的舒张反应主要由一氧化氮（NO）介导。在本研究中，我们检测了冷暴露（24摄氏度）对离体犬鼻黏膜中氮氧化物能神经介导的血管舒张的影响。从犬鼻中隔制备的鼻黏膜条，在阿托品和胍乙啶存在的情况下用甲氧明适度预收缩后，对跨壁电刺激（持续时间0.5毫秒的方波脉冲，频率5赫兹，电压25伏）产生舒张反应。24摄氏度时的舒张程度（为甲氧明诱导收缩的55.4±13.2%，平均值±标准差，n = 6）显著大于34摄氏度时的舒张程度（33.8±8.6%，n = 6）。这种现象是可逆的。相比之下，冷暴露并未改变对NO供体（0.1和1微摩尔的硝普钠）的舒张反应幅度。这些结果表明，冷暴露会增强氮氧化物能神经末梢释放NO，从而增强鼻血管的舒张，进而导致寒冷条件下鼻黏膜肿胀。
