Vidruk E H
J Appl Physiol (1985). 1985 Sep;59(3):941-6. doi: 10.1152/jappl.1985.59.3.941.
The reflex tracheomotor responses of in situ isolated segments of the extrathoracic trachea of anesthetized, paralyzed, and ventilated dogs were monitored. Reflex tracheal constriction was evoked by passive lung deflation. The purpose of this study was to determine whether the prevailing state of oxygenation altered the magnitude of this reflex. Compared with the magnitude of the response during normoxia [arterial O2 tension (PaO2) = 78 Torr], that during hypoxia (PaO2 = 44 Torr) was nearly threefold larger while that during hyperoxia (PaO2 greater than 250 Torr) was about 50% smaller. The isocapnic changes in oxygenation by themselves usually had no effect on tracheomotor tone. The deflation-induced reflex tracheal constriction was eliminated by complete denervation of the tracheal segment but usually only diminished by partial denervation. Bilateral vagotomies or bilateral carotid body denervation also usually decreased the magnitude of the reflex. It appears that the magnitude of this reflex is dependent on the prevailing state of oxygenation and that a pulmonary stretch receptor-carotid body chemoreceptor interaction accounts for the exaggerated reflex tracheal constriction during hypoxia and the attenuated response during hyperoxia.
对麻醉、麻痹并进行通气的犬的胸外气管原位分离节段的反射性气管运动反应进行了监测。被动肺萎陷可诱发反射性气管收缩。本研究的目的是确定氧合的主导状态是否会改变这种反射的强度。与常氧状态下[动脉血氧张力（PaO2）= 78托]的反应强度相比，低氧状态下（PaO2 = 44托）的反应强度几乎大三倍，而高氧状态下（PaO2大于250托）的反应强度则小约50%。等碳酸血症时氧合的变化本身通常对气管运动张力没有影响。气管节段完全去神经支配可消除放气诱发的反射性气管收缩，但部分去神经支配通常只会使其减弱。双侧迷走神经切断术或双侧颈动脉体去神经支配通常也会降低反射的强度。看来这种反射的强度取决于氧合的主导状态，并且肺牵张感受器 - 颈动脉体化学感受器相互作用解释了低氧期间反射性气管收缩的增强以及高氧期间反应的减弱。
