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一氧化氮能神经通路在豚鼠支气管收缩时反射性气管扩张中的作用

Involvement of NO-ergic neural pathway in reflex tracheal dilatation during bronchoconstriction in guinea pigs.

作者信息

Takahashi Y, Ohno H, Misawa M

机构信息

Department of Pharmacology, SS Pharmaceutical Co., Ltd., Chiba, Japan.

出版信息

Res Commun Mol Pathol Pharmacol. 1996 Sep;93(3):289-99.

PMID:8896041
Abstract

The involvement of NOergic nerve in vagal reflex-mediated tracheal dilatation during bronchoconstriction was investigated using the guinea pig in vivo tracheo-bronchi separated preparation. Inhalation of 0.01% histamine to the bronchial site induced a biphasic, vagal reflex tracheal response, i.e., constriction followed by dilatation slightly after bronchial constriction. The reflex tracheal dilatation was inhibited by 49% by local treatment of the tracheal site with 1% propranolol. The residual dilatation in the presence of atropine and propranolol was significantly inhibited by 1% oxyhemoglobin or 1% carboxy-PTIO, NO scavengers. Cyclic GMP content in the tissue of the tracheal site during the reflex tracheal dilatation significantly increased. The increase in cyclic GMP was reduced by treatment of the tracheal site with 1% N omega-nitro-L-arginine methyl ester. These results support a hypothesis that reflex tracheal dilatation during bronchoconstriction may be mediated by not only adrenergic but also NOergic nerves in guinea pigs.

摘要

使用豚鼠体内气管 - 支气管分离制备模型,研究了在支气管收缩过程中,含一氧化氮(NO)能神经参与迷走神经反射介导的气管扩张的情况。向支气管部位吸入0.01%组胺可诱发双相性的、迷走神经反射性气管反应,即支气管收缩后稍晚出现收缩继之以扩张。用1%普萘洛尔局部处理气管部位,反射性气管扩张受到49%的抑制。在阿托品和普萘洛尔存在的情况下,残余的扩张被1%氧合血红蛋白或1%羧基 - PTIO(NO清除剂)显著抑制。反射性气管扩张期间气管部位组织中的环磷酸鸟苷(cGMP)含量显著增加。用1%Nω - 硝基 - L - 精氨酸甲酯处理气管部位可使cGMP的增加减少。这些结果支持这样一种假说,即在豚鼠中,支气管收缩期间反射性气管扩张可能不仅由肾上腺素能神经介导,也由NO能神经介导。

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