Koley J, Ghosh T K, Koley B
Department of Physiology, University of Calcutta University College of Sciences, India.
Acta Physiol Hung. 1990;75(1):77-89.
Intravenous nicotine (20-60 micrograms/kg) produced an initial brief apnoea followed by hyperventilation in anaesthetized cats. The apneic response to nicotine remained uneffected by atropine, by phentolamine or propranolol. Hexamethonium and guanethedine sulphate antagonized the apneic response. In bilateral vagotomized cats, nicotine failed to produce respiratory apnoea. Veratridine and phenyldiguanide produced apnoea similar to that produced by nicotine within 2-3 sec. administered intraartrially. Nicotine failed to stimulate pulmonary stretch receptors as did veratridine in artificially ventilated cats. The alpha and gamma motoneurone activity of inspiratory and expiratory muscles and the phrenic efferent activity were inhibited during apnoea. These inhibitions were absent in vagotomized cats. In conclusion, these results suggest that the nicotine induced apneic response is mediated through pulmonary vagal afferents, probably through J-receptors, which in turn inhibit the motoneurone activity involving the respiratory muscles.
静脉注射尼古丁(20 - 60微克/千克)可使麻醉猫先出现短暂呼吸暂停,随后出现通气过度。对尼古丁的呼吸暂停反应不受阿托品、酚妥拉明或普萘洛尔的影响。六甲铵和硫酸胍乙啶可拮抗呼吸暂停反应。在双侧迷走神经切断的猫中,尼古丁未能产生呼吸暂停。藜芦碱和苯基双胍经动脉内给药后2 - 3秒内可产生与尼古丁相似的呼吸暂停。在人工通气的猫中,尼古丁不像藜芦碱那样能刺激肺牵张感受器。呼吸暂停期间,吸气和呼气肌的α和γ运动神经元活动以及膈传出活动受到抑制。在迷走神经切断的猫中不存在这些抑制作用。总之,这些结果表明,尼古丁诱导的呼吸暂停反应是通过肺迷走传入神经介导的,可能是通过J受体,进而抑制涉及呼吸肌的运动神经元活动。