哮喘联盟

   摘要
   背景和研究目的：尼古丁（NIC）作用于外周系统导致咳嗽，我们拟通过本研究验证尼古丁可作用于中枢系统抑制咳嗽反射的假设。
   试验方法：将33只猫进行戊巴比妥钠麻醉，保持自主呼吸。将尼古丁通过脊椎动脉注入呼吸脑干循环（ia），或通过显微注射法注入尾端腹部呼吸柱区域。分析并比较注射尼古丁后、对照期以及恢复期间气管支气管机械刺激下的咳嗽次数、隔膜的振幅、腹肌及喉肌的肌电图以及几项咳嗽的时间性特征。
   主要结果： (-)NIC（ia）可减少咳嗽次数、降低咳嗽力度、降低血压以及心率，且以上效应均呈剂量依赖性。(-) NICI不改变咳嗽运动模式的时间性特征。提前使用美卡拉明可缓解(-) NIC对血压和心率的影响，但并不抑制尼古丁的止咳功能。(+) NIC在抑制咳嗽方面的功能较(-) NIC弱。显微注射(-) NIC至尾端腹部呼吸柱区域对咳嗽的抑制作用与ia方式类似。在该区域显微注射美卡拉明后立即注射尼古丁不显著降低能尼古丁的咳嗽抑制作用。
   结论和提示：尼古丁乙酰胆碱受体在调节脑干功能方面发挥重要作用，尤其是针对尾端腹部呼吸柱区域的与气管支气管咳嗽反射相关的神经元，并且该机制对美卡拉明不敏感。
 

（刘国梁 审校）
 JApplPhysiol(1985).2014Dec4:jap.00075.2014.doi:10.1152/japplphysiol.00075.2014. [Epub ahead of print]


 

Central administration of nicotine suppresses tracheobronchial cough in anesthetized cats.
 

Poliacek I1, Rose MJ2, Pitts TE3, Mortensen A4, Corrie LW2, Davenport PW3, Bolser DC2.
 

ABSTRACT
BACKGROUND AND PURPOSE：We tested the hypothesis that nicotine (NIC), which acts peripherally to promote coughing, might inhibit reflex cough at a central site.
EXPERIMENTAL APPROACH：NIC was administered via the vertebral artery (ia) to the brainstem circulation and by microinjections into a restricted area of the caudal ventral respiratory column in 33 pentobarbital anesthetized spontaneously breathing cats. The number of coughs induced by mechanical stimulation of the tracheobronchial airways, amplitudes of the diaphragm, abdominal muscle, and laryngeal muscles EMGs, and several temporal characteristics of cough were analyzed after administration of NIC and compared to those during control and recovery period.
KEY RESULTS：(-) NIC (ia) reduced cough number, cough expiratory efforts, blood pressure, and heart rate in a dose-dependent manner. (-) NIC did not alter temporal characteristics of the cough motor pattern. Pretreatment with mecamylamine prevented the effect of (-) NIC on blood pressure and heart rate, but did not block the antitussive action of this drug. (+) NIC was less potent than (-) NIC for inhibition of cough. Microinjections of (-) NIC into the caudal ventral respiratory column produced similar inhibitory effects on cough as administration of this isomer by the ia route. Mecamylamine microinjected in the region just before nicotine did not significantly reduce the cough suppressant effect of nicotine.
CONCLUSIONS AND IMPLICATIONS：Nicotinic acetylcholine receptors significantly modulate functions of brainstem and in particular caudal ventral respiratory column neurons involved in expression of the tracheobronchial cough reflex by a mecamylamine insensitive mechanism.
 

JApplPhysiol(1985).2014Dec4:jap.00075.2014.doi:10.1152/japplphysiol.00075.2014. [Epub ahead of print]