Mechanisms underlying stimulation of rapidly adapting receptors during pulmonary air embolism in dogs.
We investigated the mechanisms underlying stimulation of rapidly adapting receptors (RARs) during pulmonary air embolism (PAE). Impulses were recorded from RARs in 43 anesthetized, open-chest and artificially ventilated dogs. Forty one out of 56 RARs were stimulated by infusion of air into the right atrium (0.2 ml/kg per min for 10 min). As a group (n = 56), RAR activity increased from a baseline of 1.2 +/- 0.2 to a peak of 4.3 +/- 0.3 impulses/breath at 8-10 min after the onset of PAE induction. PAE also caused an increase in total lung resistance and a decrease in dynamic lung compliance. Studies were repeated in 33 RARs initially stimulated by PAE. In nine receptors, hyperinflation of the lungs performed at the termination of the second PAE induction largely reversed both the afferent and bronchomotor responses. Furthermore, the residual PAE-evoked activity subsequent to hyperinflation was almost eliminated by elevation in the heart position. In another 24 receptors, the responses of RARs to PAE were unaltered by pretreatment with saline (n = 8) or dimethylthiourea (a hydroxyl radical scavenger; n = 8), but was significantly attenuated by pretreatment with ibuprofen (a cyclooxygenase inhibitor: n = 8). These results suggest that: (1) the increased RAR activity following PAE is associated primarily with an increase in bronchomotor tone and secondarily with the mechanical action of the beating heart impacting on lung tissues; and (2) cyclooxygenase products may be involved in this sensory stimulation.