Hypercapnia and hypoxia which develop during retching participate in the transition from retching to expulsion in dogs.

The roles of arterial and central chemoreceptors in the transition from retching to expulsion during vomiting were studied. In spontaneously breathing decerebrate dogs, actual vomiting induced by activation of abdominal vagal afferents always consisted of retching and subsequent expulsion phases. Pulmonary ventilation almost stopped during the retching phase. Arterial blood CO2 tension gradually increased and reached a maximum near the time of the transition from the retching phase to the expulsion phase. Similarly, when end-tidal CO2 was maintained higher than 4.6 +/- 0.7% in paralyzed, artificially ventilated decerebrate dogs, stimulation of abdominal vagal afferents induced fictive retching and fictive expulsion, which were identified from the characteristic discharge patterns of the motor nerves to the costal and hiatal parts of the diaphragm, the abdominal muscles and the digastric muscle. However, only fictive retching occurred at an end-tidal CO2 of less than 3.7 +/- 0.7%. Although end-tidal CO2 was at a low level, fictive retching was followed by fictive expulsion when artificial ventilation was interrupted during the fictive retching phase and when sinus nerve afferents were stimulated. Even after sino-aortic denervation, fictive retching and subsequent fictive expulsion could be induced by stimulation of either vagal afferents or the solitary tract and nucleus, but the threshold level of end-tidal CO2 which enabled the induction of fictive expulsion increased after denervation. These results indicate that the activity of arterial and/or central chemoreceptor afferents must exceed some critical level to induce the transition from the retching phase to the expulsion phase.