Lindberg S, Hybbinette J C, Mercke U
Eur J Respir Dis. 1985 Jan;66(1):40-6.
The in vivo effect of nicotine bitartrate on mucociliary (mc) activity in the rabbit maxillary sinus was investigated. An animal model was used, which permitted administration of drugs directly into the artery feeding the sinus and simultaneous recording of changes in the mc activity. When nicotine was given ia (0.5-10.0 micrograms/kg) it resulted in a brief (1 min at most) acceleration of the mc wave frequency. The response was dose-dependent and a maximum increase of 34.9% was recorded at a dose of 10.0 micrograms/kg. The response was inhibited by a preceding injection of the ganglionic blocker hexamethonium (0.2 mg/kg) or the cholinergic antagonist atropine (0.2 mg/kg). The alpha and beta-adrenoceptor antagonists phentolamine (0.2 mg/kg) and propranolol (0.2 mg/kg) did not influence the response to nicotine injection. It is concluded that the acceleration of mc wave frequency after nicotine administration is probably mediated via stimulation of nicotinic receptors on postganglionic parasympathetic nerve cells.
研究了酒石酸尼古丁对兔上颌窦黏膜纤毛（mc）活性的体内效应。采用了一种动物模型，该模型允许将药物直接注入供应窦的动脉，并同时记录mc活性的变化。当经动脉注射尼古丁（0.5 - 10.0微克/千克）时，可导致mc波频率短暂（最多1分钟）加速。该反应呈剂量依赖性，在剂量为10.0微克/千克时记录到最大增加34.9%。预先注射神经节阻滞剂六甲铵（0.2毫克/千克）或胆碱能拮抗剂阿托品（0.2毫克/千克）可抑制该反应。α和β肾上腺素能受体拮抗剂酚妥拉明（0.2毫克/千克）和普萘洛尔（0.2毫克/千克）不影响对尼古丁注射的反应。得出的结论是，尼古丁给药后mc波频率的加速可能是通过刺激节后副交感神经细胞上的烟碱受体介导的。
