Takahashi Y, Ohno H, Misawa M
Department of Pharmacology, SS Pharmaceutical Co., Ltd., Narita, Japan.
Eur J Pharmacol. 1996 Apr 29;302(1-3):89-97. doi: 10.1016/0014-2999(96)00017-9.
The reflex tracheal response induced by bronchoconstriction was investigated using a newly devised tracheo-bronchi preparation in anesthetized guinea pigs. Tracheal constriction and subsequent dilatation were observed in response to bronchoconstriction induced by the inhalation of 0.001-0.01% histamine and 0.003-0.03% acetylcholine. These tracheal responses were abolished by cervical vagotomy or treatment of the tracheal site with 1% tetrodotoxin. Tracheal constriction and dilatation were significantly inhibited by 0.1% atropine and 1% propranolol, respectively. When high tracheal tone was induced by 0.01% serotonin, the residual tracheal dilatation observed in the presence of propranolol was enhanced, while dilatation was completely inhibited by 1% hexamethonium. Dilatation was also suppressed by 1% N omega-nitro-L-arginine methyl ester (L-NAME) and 1% methylene blue. The tracheal constriction produced by bronchoconstriction was significantly enhanced by propranolol 2 mg/kg, i.v. and L-NAME 10 mg/kg, i.v. These results demonstrate that a vagally mediated reflex tracheal response (constriction followed by dilatation) is induced by bronchoconstriction in anesthetized guinea pigs. Cholinergic nerves may mediate the constriction, and adrenergic and nonadrenergic noncholinergic (NANC) inhibitory nerves may mediate the dilatation. Furthermore, NO may be involved in the NANC reflex tracheal dilatation.
利用一种新设计的气管 - 支气管标本，在麻醉的豚鼠身上研究了支气管收缩诱导的反射性气管反应。吸入0.001 - 0.01%组胺和0.003 - 0.03%乙酰胆碱诱导支气管收缩后，观察到气管收缩及随后的扩张。这些气管反应可通过颈迷走神经切断术或用1%河豚毒素处理气管部位而消除。气管收缩和扩张分别被0.1%阿托品和1%普萘洛尔显著抑制。当用0.01%血清素诱导高气管张力时，在普萘洛尔存在下观察到的残余气管扩张增强，而扩张被1%六甲铵完全抑制。扩张也被1% Nω - 硝基 - L - 精氨酸甲酯（L - NAME）和1%亚甲蓝抑制。静脉注射2 mg/kg普萘洛尔和10 mg/kg L - NAME可显著增强支气管收缩引起的气管收缩。这些结果表明，在麻醉的豚鼠中，支气管收缩可诱导迷走神经介导的反射性气管反应（收缩后扩张）。胆碱能神经可能介导收缩，而肾上腺素能和非肾上腺素能非胆碱能（NANC）抑制性神经可能介导扩张。此外，NO可能参与NANC反射性气管扩张。
