Role of Vagal nerve in Airway Hyperresponsiveness.

虽然迷走神经在支气管哮喘发病机制中的重要性已被报道，但其确切的贡献仍未完全了解。为了更清楚地了解这一领域，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）中的可能作用，并确定了组胺对迷走神经的作用部位。为此，我们研究了麻醉和机械通气豚鼠双侧宫颈迷走神经切除术、六甲铵（2mg /kg）或河豚毒素（0.5 mg/kg）对HIB （8 mg/kg, iv）的影响。我们还研究了阿托品（1mg /kg）是否能降低迷走神经切除术后的HIB，包括六甲铵或河豚毒素治疗。得到以下结果：1)迷走神经切开术、六甲铵或河豚毒素均显著增强组胺反应。(2)心得安可增加HIB，迷走神经切开术可进一步提高HIB。3)阿托品能显著抑制迷走神经切断术、六甲铵和河豚毒素后的HIB。这些结果提示神经节后迷走神经通过神经末梢释放乙酰胆碱在HIB中起兴奋作用。同时也提示迷走神经反射在豚鼠HIB中主要表现出抑制作用，可能是第二种，为了阐明局部反射是否可能释放速激肽，我们在体外研究了阿托品（10^<-6> M）、河河毒素（TTX） （10^<-7> M）对缓激肽诱导的豚鼠气管平滑肌（TSM）收缩的影响，并进行了辣椒素预处理和不预处理。在对照动物中，阿托品未改变缓激肽引起的收缩。TTX抑制缓激肽诱导的收缩。在辣椒素预处理的动物中，阿托品和TTX均未影响缓激肽诱导的TSM收缩。这些结果表明，缓激肽可能引起局部神经介导的TSM收缩作用，而不释放迷走神经输出末梢的乙酰胆碱，可能是通过轴突反射从迷走神经输出末梢释放速激肽。少

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