Baker J P, Frazier D T, Hanley M, Zechman F W
Respir Physiol. 1979 Apr;36(3):337-51. doi: 10.1016/0034-5687(79)90046-x.
The response of medullary expiratory neurons to added mechanical and chemical loads was studied in anesthetized cats. Alterations in burst characteristics and central timing were compared in the intact and bilaterally vagotomized cat. The following results were obtained: (1) Graded expiratory airflow resistances caused progressive increases in burst duration, spikes per burst and firing rate; similar effects were noted for end-inspiratory tracheal occlusions and continuous positive breathing; all facilitation was eliminated by vagotomy. (2) Graded inspiratory airflow resistances delayed the onset of an expiratory burst but did not change the overall burst characteristics. (3) Acute hypercapnia increased ventilation without noticeable changes in expiratory burst characteristics; acute hypoxia produced a reduction in burst duration concomitant with changes in ventilation. It is concluded that (1) expiratory neurons are responsive to vagally mediated volume information and (2) transient hypoxia and hypercapnia sufficient to increase ventilation does not increase the firing rate of expiratory neurons but exerts differential effects with respect to timing. It is suggested that expiratory duration is related to the time integral of expired volume and that the increase in FRC imposed by expiratory loads does not alter the central timing of the next inspiration.
在麻醉猫身上研究了延髓呼气神经元对增加的机械和化学负荷的反应。比较了完整猫和双侧迷走神经切断猫的爆发特性和中枢定时的变化。得到以下结果:(1) 分级呼气气流阻力导致爆发持续时间、每次爆发的尖峰数和放电频率逐渐增加;吸气末气管阻塞和持续正压通气也有类似作用;迷走神经切断消除了所有促进作用。(2) 分级吸气气流阻力延迟了呼气爆发的开始,但没有改变整体爆发特性。(3) 急性高碳酸血症增加通气,但呼气爆发特性无明显变化;急性缺氧导致爆发持续时间缩短,同时通气发生变化。得出结论:(1) 呼气神经元对迷走神经介导的容量信息有反应;(2) 足以增加通气的短暂缺氧和高碳酸血症不会增加呼气神经元的放电频率,但在定时方面有不同作用。提示呼气持续时间与呼出气体量的时间积分有关,呼气负荷引起的功能残气量增加不会改变下一次吸气的中枢定时。