EFFECTS OF PULMONARY AIR-EMBOLISM ON DISCHARGE OF SLOWLY ADAPTING PULMONARY STRETCH RECEPTORS

Pulmonary air embolism (PAE) usually causes small-airway collapse. Loc al transpulmonary pressure (Ptr) is thought to be closely associated w ith the activity of slowly adapting pulmonary stretch receptors (SAPSR s). To test whether discharge of SAPSRs located distal to collapsed ai rways is closely related to the overall Ptr, we studied 65 SAPSRs in a nesthetized paralyzed open-chest dogs that were ventilated at constant tidal volume and frequency. PAE increased both Ptr and total pulmonar y resistance but decreased dynamic lung compliance. Three groups of SA PSRs were identified on the basis of their locations in intrapulmonary airways. Group I had 29 SAPSRs located in airways <1 mm in diameter. Group II had 10 SAPSRs that were found in intrapulmonary airways betwe en 1 and 2 mm in diameter. PAE decreased the activity of 31 of the 39 SAPSRs in these two groups. Their activity during PAE was not related to Ptr. The 26 SAPSRs in group III were in airways >2 mm in diameter. PAE increased the peak firing rate of 18 of these receptors, and there was a close relationship between the discharge frequency of these SAP SRs and the Ptr during PAE. In groups I and II, the dissociation betwe en Ptr and SAPSR activity during PAE may have been caused by periphera l airway collapse. Activity of central fibers was blocked at higher te mperatures than activity of peripheral fibers. We suggest that the res ponse of a SAPSR to PAE depends on the location of the receptor within the lungs, and we speculate that threshold and fiber type are also re lated to location.