Transient responses of pulmonary stretch receptors in the dog to inhalation of carbon dioxide

Abstract

The transient response to hypercapnia (8% CO 2 in O 2) has been studied for 22 pulmonary stretch receptors in 12 dogs, anaesthetized and artificially ventilated, in which the end-tidal CO 2 was maintained at 15 mm Hg. Hypercapnia inhibited the activity of the stretch receptors ; the time course of this inhibition was slower for stretch receptors localized in the larger extrapulmonary airways than for those localized in the smaller intrapulmonary airways. The maximum inhibition occurred after 16 sec and 90 sec for receptors placed in the intrapulmonary and extrapulmonary airways, respectively; the mean frequency of discharge was reduced in both eases to 75% of that of the control breaths. The inhibitory effect of CO 2 was found to be significantly greater in the intrapulmonary receptors after ligature of the pulmonary artery. These effects do not seem to be due to a variation of the bronchomotor tone since they were not influenced by the administration of isoprenaline. The results are interpreted rather as responses to local variation of H + concentration since the administration of acetazolamide was found to block the eflects of CO 2 on the discharge of stretch receptors. These results might suggest the existence of a mechanism partially responsible for the ventilatory response to carbon dioxide.