Communications

Abstract

It has been reported that changes of intrapulmonary CO2 in the dog alter ventilation, via the vagus nerve (Bartoli et al. 1974; Banzett et al. 1978). An attempt was made to quantitate this CO2 reflex through a range of intrapulmonary CO2 and airway pressure (Paw) levels.Dogs were anaesthetized with chloralose-urethane (initial dose 350 mg urethane, 110 mg chloralose per kg; continuous infusion of half that dose per hour) and paralysed with Flaxedil (7 mg/kg). The chest was opened and a blocking catheter was placed in the main bronchus of the left lung to allow independent but synchronous ventilation of both lungs by a dual-piston pump. The left lung was vascularly isolated by externally occluding the left pulmonary artery, adequate gas exchange was maintained by the right lung, which was vagally denervated. Thus, arterial blood gases could be held constant during experimental manoeuvres. Efferent activity from the C5 root of the phrenic nerve was recorded and integrated as described by Bartoli et al. (1975).In the vascularly isolated lung, various constant levels of CO2, between 1 and 8 %, were attained and the integrated phrenic signal recorded both during phasic changes in Pw at different end-expiratory loads (between 3 and 7 cm H20) and at different levels of static lung inflation (Paw between 4 and 16 cm H20).Both phasic and static lung inflation resulted in a rhythmic pattern of phrenic nerve activity. Alterations in end-expiratory load or in static Pw were reflected in changes of this pattern, the predominant effect with increasing lung pressure being a prolongation of TE (time from peak discharge to onset of the next phrenic burst).We did not detect any consistent influence of lung CO2 on the relationship between static Paw and phrenic nerve activity. With phasic lung inflation effects of CO2 on the integrated phrenic signal were only observed when lung CO2 was below 1-5 %. These effects were, however, invariably associated with changes in peak Paw Above 1-5 % CO2 changes were not observed in the integrated phrenic signal.The results indicate that a decrease in ventilatory drive may be induced only with reduction in CO2 to low levels and suggest that lung mechanics may play a significant role in the underlying mechanism.