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Role of Vagal nerve in Airway Hyperresponsiveness.

迷走神经在气道高反应性中的作用。

基本信息

批准号：
01570432
负责人：
AIZAWA Hisamichi
金额：
$ 1.41万
依托单位：
Kyushu University
依托单位国家：
日本
项目类别：
Grant-in-Aid for General Scientific Research (C)
财政年份：
1989
资助国家：
日本
起止时间：
1989 至 1990
项目状态：
已结题

项目摘要

Although the importance of the vagal nerve in the pathogenesis of bronchial asthma has been reported, its precise contribution is still not fully understood. To shed more light on this area, we performed the following experiments.First, we evaluated the possible contribution of vagal reflex in Histamine-Induced Bronchoconstriction (HIB), and decided the site of action of histamine on the vagal nerve. For this purpose, we studied the effects of the bilateral cervical vagotomy, hexamethonium (2 mg/kg) or tetrodotox in (0.5 mg/kg) on HIB (8 mug/kg, iv) in anesthetized and mechanically ventilated guinea pigs. We also studied whether or not atropine (1 mg/kg) decreases HIB after vagotomy, including either the treatment of hexamethonium or tetrodotoxin.The following results were obtained ; 1) The response to histamine was significantly enhanced by the vagotomy, hexamethonium or tetrodotoxin. 2) Propranolol increased HIB and HIB was further enhanced by the vagotomy in the animals treated with … More propranolol. 3) Atropine significantly suppressed HIB after the vagotomy, hexamethonium or tetrodotoxin. These results suggest that the postganglionic vagus nerve plays an excitatory role in HIB through the release of acetylcholine from the nerve terminals. It is also suggested that the vagal reflex mainly exhibits an inhibitory role in the HIB of guinea pigs, presumably by theSecond, to elucidate whether the local reflex may release tachykinin, we studied the effects of atropine (10^<-6> M), tetrodotoxin (TTX) (10^<-7> M) on the bradykinin induced contraction of guinea pig Tracheal Smooth Muscle (TSM) in vitro, with or without capsaicin pretreatment. Atropine did not change the contraction induced by bradykinin in the control animals. TTX suppressed bradykinin-induced contraction. Neither atropine nor TTX did affect bradykinin-induced contraction of TSM in the animals with capsaicin pretreatment.These results indicated that bradykinin may cause a local neurally mediated action in TSM contraction, without release of acetylcholine from efferent vagal nerve terminals, presumably by the release of tachykinins from vagal efferent endings through axon reflex. Less

尽管迷走神经在支气管哮喘发病机制中的重要性已有报道，但其确切贡献仍不完全清楚。为了进一步阐明这一领域，我们进行了以下实验。首先，我们评估了迷走神经反射在组胺诱导的支气管收缩（HIB）中可能的贡献，并确定了组胺对迷走神经的作用部位。为此，我们研究了双侧颈部迷走神经切断术、六甲铵（2 mg/kg）或河豚毒素（0.5 mg/kg）对麻醉和机械通气豚鼠的 HIB（8 杯/kg，静脉注射）的影响。我们还研究了阿托品 (1 mg/kg) 是否会降低迷走神经切断术后的 HIB，包括六甲铵或河豚毒素治疗。获得了以下结果； 1) 迷走神经切断术、六甲铵或河豚毒素显着增强对组胺的反应。 2) 普萘洛尔增加了 HIB，而用普萘洛尔治疗的动物的迷走神经切断术进一步增强了 HIB。 3)阿托品、六甲铵或河豚毒素在迷走神经切断术后显着抑制HIB。这些结果表明节后迷走神经通过神经末梢释放乙酰胆碱在 HIB 中发挥兴奋作用。也有人认为，迷走神经反射主要对豚鼠的HIB表现出抑制作用，推测是由该反射引起的。其次，为了阐明该局部反射是否可能释放速激肽，我们研究了阿托品(10^<-6>M)、河豚毒素(TTX)(10^<-7>M)对缓激肽引起的豚鼠气管平滑肌收缩的影响。体外肌肉 (TSM)，有或没有辣椒素预处理。阿托品没有改变对照动物中缓激肽诱导的收缩。 TTX 抑制缓激肽诱导的收缩。在用辣椒素预处理的动物中，阿托品和 TTX 都不影响缓激肽诱导的 TSM 收缩。这些结果表明，缓激肽可能在 TSM 收缩中引起局部神经介导的作用，而不从迷走神经传出神经末梢释放乙酰胆碱，可能是通过轴突反射从迷走神经传出末梢释放速激肽。较少的