Takeda R, Haji A
Department of Pharmacology, Faculty of Medicine, Toyama Medical and Pharmaceutical University, Japan.
Jpn J Pharmacol. 1993 May;62(1):57-65. doi: 10.1254/jjp.62.57.
Effects of isoflurane on the membrane potential trajectory and synaptic activity in bulbar respiratory neurons were investigated in decerebrate, vagotomized and artificially ventilated cats. A 2-min inhalation of 1.6% end-tidal concentration of isoflurane produced depolarization of the membrane in 10 out of 18 inspiratory, 8 out of 15 post-inspiratory and 5 out of 12 expiratory neurons and hyperpolarization in the rest of the population recorded in the ventral respiratory group. In both depolarized and hyperpolarized cells, periodically occurring excitatory and inhibitory synaptic waves were decreased, and input resistance was increased. Concomitantly, isoflurane reduced the excitatory and inhibitory postsynaptic potentials evoked by electrical stimulation of the vagus nerve, superior laryngeal nerve and cervical spinal cord. The effects of isoflurane on membrane potential and input resistance became negligible when excitatory and inhibitory synaptic potentials were suppressed by iontophoretically applied tetrodotoxin. The present results suggest that the respiratory neuronal responses induced by isoflurane are attributed mainly to the decrease of excitatory and inhibitory synaptic interactions in the bulbar respiratory network of neurons.
在去大脑、切断迷走神经并人工通气的猫身上，研究了异氟烷对延髓呼吸神经元膜电位轨迹和突触活动的影响。吸入2分钟呼气末浓度为1.6%的异氟烷后，腹侧呼吸组记录的18个吸气神经元中有10个、15个吸气后神经元中有8个、12个呼气神经元中有5个出现膜去极化，其余神经元出现超极化。在去极化和超极化细胞中，周期性出现的兴奋性和抑制性突触波均减少，输入电阻增加。同时，异氟烷降低了电刺激迷走神经、喉上神经和颈脊髓所诱发的兴奋性和抑制性突触后电位。当通过离子导入法应用河豚毒素抑制兴奋性和抑制性突触电位时，异氟烷对膜电位和输入电阻的影响可忽略不计。目前的结果表明，异氟烷诱导的呼吸神经元反应主要归因于延髓呼吸神经元网络中兴奋性和抑制性突触相互作用的减少。
