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Transient lung inflation increased the volume of a bypassed tracheal segment in anesthetized dogs, whether spontaneously breathing or paralyzed and artificially ventilated. The degree of dilation during inflation varied with the state of “tone” of the tracheal muscle and with the inflation volume. Pulmonary denervation caused maintained constriction of the trachea and blocked the dilation during lung inflation. Cooling the cervical vagus nerves to between 7 and 12 C had the same effect. Both of these procedures blocked the Hering-Breuer inflation reflex, but the trachea still constricted following carotid body chemoreceptor stimulation by KCN. In paralyzed dogs, injection of veratrine into the right heart caused tracheal dilation, presumably by stimulating pulmonary stretch receptors. Left heart injection dilated the trachea much less. The former effect was abolished by pulmonary denervation. In anesthetized spontaneously breathing dogs carotid body chemoreceptor stimulation by KCN constricted the trachea; this was followed by increased ventilation and secondary tracheal dilation. Pulmonary denervation or muscular paralysis and artificial ventilation prevented the secondary dilation. These results establish the reflex nature of tracheal dilation during transient lung inflation and suggest that Hering-Breuer stretch receptors are the responsible end organs. Submitted on January 15, 1963
Widdicombe et al. (Mon,) studied this question.