Dawid-Milner M S, Lara J P, Gonzaléz-Barón S, Spyer K M
Departamento de Fisiología, Facultad de Medicina, Universidad de Málaga, Spain.
Pflugers Arch. 2001 Jan;441(4):434-43. doi: 10.1007/s004240000450.
To assess the importance of the pontine A5 region in modulating respiratory activity, electric current or microinjections of glutamate (10-30 nl, 1-3 nmol) were used to stimulate discrete zones within this region in the spontaneously breathing, anaesthetised rat. These stimuli evoked an expiratory facilitatory response, consisting of a decrease in respiratory rate (P < 0.01 electrical, P < 0.001 chemical) due to an increase of expiratory time (P < 0.01 in both cases) as measured from recordings of phrenic nerve activity. No changes were observed in inspiratory time. To avoid changes in PCO2, which could modulate the respiratory response, stimulation was also made during artificial ventilation. Under these conditions the expiratory facilitatory response elicited by glutamate was still present (P < 0.05), although its duration was reduced (P < 0.05), as was the magnitude of the phrenic burst (P < 0.05). At all the sites at which electrical stimulation and glutamate injection had evoked a respiratory response, electrical stimulation evoked a concomitant increase in both blood pressure and heart rate. Glutamate injection evoked a pressor response in 21 out of 30 animals. In eight animals the rise in blood pressure was followed by a fall in blood pressure and in one animal, a depressor response was observed. In all cases glutamate evoked an increase in heart rate. The expiratory facilitatory response was not evoked as a consequence of the increase of blood pressure since it was still present after the administration of guanethidine, which abolished the blood pressure changes. As glutamate is believed to excite perikarya rather than axons of passage these data indicate that expiratory facilitatory responses and the accompanying cardiovascular changes are the consequence of activating neurones located within the A5 region. The possible interactions between the A5 region and the medullary respiratory complex in eliciting these changes are discussed.
为评估脑桥A5区在调节呼吸活动中的重要性,在自主呼吸的麻醉大鼠中,使用电流或微量注射谷氨酸(10 - 30 nl,1 - 3 nmol)刺激该区域内的离散区域。这些刺激引发了呼气促进反应,表现为呼吸频率降低(电刺激时P < 0.01,化学刺激时P < 0.001),这是由于呼气时间增加(两种情况下P < 0.01),通过膈神经活动记录测量得出。吸气时间未观察到变化。为避免可调节呼吸反应的PCO2变化,在人工通气期间也进行了刺激。在这些条件下,谷氨酸引发的呼气促进反应仍然存在(P < 0.05),尽管其持续时间缩短(P < 0.05),膈神经爆发的幅度也减小(P < 0.05)。在所有电刺激和谷氨酸注射引发呼吸反应的部位,电刺激同时引起血压和心率升高。30只动物中有21只注射谷氨酸后出现升压反应。8只动物血压升高后出现血压下降,1只动物观察到降压反应。在所有情况下,谷氨酸均引起心率增加。呼气促进反应不是由血压升高引起的,因为在给予胍乙啶消除血压变化后该反应仍然存在。由于谷氨酸被认为是兴奋胞体而非过路轴突,这些数据表明呼气促进反应及伴随的心血管变化是激活A5区内神经元的结果。讨论了A5区与延髓呼吸复合体在引发这些变化过程中可能的相互作用。