Takeda R, Haji A
Department of Pharmacology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan.
Pharmacol Toxicol. 1990 Mar;66(3):190-6. doi: 10.1111/j.1600-0773.1990.tb00731.x.
The effects of ethanol on two types of bulbar expiratory neurones, post-inspiratory (early expiratory) and expiratory (late expiratory) neurones, were studied in decerebrated, paralyzed and artificially ventilated cats. Intravenous injection of ethanol (300 mg/kg) depressed the efferent activity in the phrenic and recurrent laryngeal nerves which displayed the augmenting discharge during inspiration and the decrementing discharge during the early stage of expiration (stage I expiration). It reduced the duration of expiration, with a preferential effect on stage I expiration. Out of 22 medullary respiratory neurones consisting of 14 post-inspiratory and 8 expiratory neurones, 12 neurones were depolarized by ethanol and 10 neurones were hyperpolarized. In both cases, the respiratory fluctuations of membrane potential diminished and synaptic noises decreased. Input resistances of these neurones remained unchanged. Ethanol depressed the spike activity during stage I expiration of the post-inspiratory neurones. In expiratory neurones, a suppression of firing was greater in stage I expiration than in later stages of expiration. The present results demonstrate that ethanol reduces the expiratory period mainly through the depression of the post-inspiratory neuronal activity in the bulbar respiratory control mechanism.
在去大脑、麻痹并进行人工通气的猫身上，研究了乙醇对两种延髓呼气神经元，即吸气后（早期呼气）神经元和呼气（晚期呼气）神经元的影响。静脉注射乙醇（300毫克/千克）抑制了膈神经和喉返神经的传出活动，这些神经在吸气时放电增强，在呼气早期（呼气第一阶段）放电减少。它缩短了呼气持续时间，对呼气第一阶段有优先作用。在由14个吸气后神经元和8个呼气神经元组成的22个延髓呼吸神经元中，12个神经元被乙醇去极化，10个神经元被超极化。在这两种情况下，膜电位的呼吸波动减小，突触噪声降低。这些神经元的输入电阻保持不变。乙醇抑制了吸气后神经元在呼气第一阶段的锋电位活动。在呼气神经元中，呼气第一阶段的放电抑制比呼气后期更大。目前的结果表明，乙醇主要通过抑制延髓呼吸控制机制中吸气后神经元的活动来缩短呼气期。
