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猫气道中非肾上腺素能非胆碱能抑制性神经系统的反射激活。

Reflex activation of the nonadrenergic noncholinergic inhibitory nervous system in feline airways.

作者信息

Szarek J L, Gillespie M N, Altiere R J, Diamond L

出版信息

Am Rev Respir Dis. 1986 Jun;133(6):1159-62. doi: 10.1164/arrd.1986.133.6.1159.

Abstract

Experiments were undertaken to learn if the nonadrenergic noncholinergic inhibitory nervous system (NANCIS) in feline airways could be activated reflexly either by mechanically stimulating the laryngeal mucosa or by inducing acute bronchospasm with boluses of 5-hydroxytryptamine (5HT) injected intravenously. Mechanical stimulation of the dorsal laryngeal mucosa evoked a biphasic bronchomotor response in anesthetized cats that had received intravenously an infusion of 5HT to raise their basal airway smooth muscle tone. The response consisted of a transient augmentation of bronchoconstriction followed by a prolonged bronchodilation. After muscarinic cholinergic receptor blockade with atropine, the constriction phase of the response disappeared, but the relaxation phase persisted. Bronchodilation elicited by laryngeal stimulation was resistant to beta-adrenergic receptor blockade with propranolol but was abolished by autonomic ganglionic blockade with hexamethonium and blocked reversibly by vagal cooling. The latter interventions, when imposed between successive dose-response curves generated by intravenous 5HT in animals pretreated with atropine and propranolol, did not alter the positions or slopes of the curves. These findings support the conclusion that mechanical stimulation of the larynx reflexly activates not only the well-known vagal cholinergic excitatory pathway to the airways but also the more recently described vagal, nonadrenergic noncholinergic inhibitory pathway. The results further indicate that bronchoconstriction is neither a prerequisite for the bronchodilator component of the laryngeal bronchomotor reflex nor an independent initiating stimulus for NANCIS-mediated reflex bronchodilation.

摘要

开展实验以了解猫气道中的非肾上腺素能非胆碱能抑制性神经系统(NANCIS)是否可通过机械刺激喉黏膜或静脉注射大剂量5-羟色胺(5HT)诱发急性支气管痉挛来反射性激活。对已静脉输注5HT以提高其基础气道平滑肌张力的麻醉猫,机械刺激喉背侧黏膜会引发双相支气管运动反应。该反应包括支气管收缩的短暂增强,随后是长时间的支气管舒张。用阿托品阻断毒蕈碱胆碱能受体后,反应的收缩期消失,但舒张期持续存在。喉刺激引起的支气管舒张对普萘洛尔的β-肾上腺素能受体阻断有抗性,但六甲铵对自主神经节的阻断可将其消除,迷走神经冷却可使其可逆性阻断。在经阿托品和普萘洛尔预处理的动物中,当在静脉注射5HT产生的连续剂量反应曲线之间进行后一种干预时,不会改变曲线的位置或斜率。这些发现支持以下结论:对喉部的机械刺激不仅可反射性激活众所周知的迷走神经胆碱能兴奋性气道通路,还可激活最近描述的迷走神经非肾上腺素能非胆碱能抑制性通路。结果还表明,支气管收缩既不是喉支气管运动反射舒张成分的先决条件,也不是NANCIS介导的反射性支气管舒张的独立起始刺激因素。

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