D'Angelo E
Respir Physiol. 1982 Feb;47(2):193-218. doi: 10.1016/0034-5687(82)90111-6.
The relation between relative peak 'integrated' diaphragmatic (Adi) and cranial (u) or caudal (1) inspiratory intercostal activity (Aic) was assessed in intact and vagotomized rabbits during rebreathing. During unloaded rebreathing Aic increased markedly more than Adi, and Aicu more than Aicl, independently of intact vagi. Vagal signals facilitated inspiratory intercostals, since vagotomy or vagal blocks increased Adi more than Aic without changing diaphragm activity time course, and delta Aic/delta Adi in the same range of Adi values was greater before than after vagotomy. Reflexes from the chest wall were not involved since phrenic block after vagotomy modified rib cage motion without changing Aic, independently of chemical drive. Possibly chemical and vagal dependent changes in fusimotor activity contribution to VT, as the latter increases. Obstruction at FRC shifted postvagotomy Aic vs. Adi relationship upwards, suggesting reflex facilitation of intercostals by chest wall receptors. The strength of this reflex was largely independent of intact vagi, since pre- and postvagotomy Aic vs. Adi relations coincided, and of chemical drive, since postvagotomy delta Aic/delta Adi for obstructed and unimpeded rebreathing were similar.
在完整和迷走神经切断的家兔再呼吸过程中，评估了相对峰值“整合”的膈肌（Adi）与头侧（u）或尾侧（1）吸气肋间肌活动（Aic）之间的关系。在无负荷再呼吸期间，Aic的增加明显超过Adi，且Aicu超过Aicl，与迷走神经是否完整无关。迷走神经信号促进吸气肋间肌，因为迷走神经切断或迷走神经阻滞使Adi的增加超过Aic，而不改变膈肌活动的时间进程，并且在相同Adi值范围内，迷走神经切断前的ΔAic/ΔAdi大于切断后。胸壁反射未参与其中，因为迷走神经切断后膈神经阻滞改变了胸廓运动，但不改变Aic，与化学驱动无关。随着潮气量（VT）增加，可能是化学和迷走神经依赖性的梭内肌活动变化导致了VT的增加。功能残气量（FRC）处的阻塞使迷走神经切断后的Aic与Adi关系向上移动，提示胸壁感受器对肋间肌有反射性促进作用。这种反射的强度在很大程度上与迷走神经是否完整无关，因为迷走神经切断前后Aic与Adi的关系一致；也与化学驱动无关，因为迷走神经切断后阻塞性和非阻塞性再呼吸的ΔAic/ΔAdi相似。
