MECHANISMS OF STIMULATION OF VAGAL PULMONARY C-FIBERS BY PULMONARY AIR-EMBOLISM IN DOGS

We investigated the involvement of the cyclooxygenase metabolites and hydroxyl radical (. OH) in the stimulation of vagal pulmonary C fibers (PCs) by pulmonary air embolism (PAE). Impulses were recorded from PC s in 51 anesthetized, open-chest, and artificially ventilated dogs. Fi fty of 59 PCs were stimulated by infusion of air into the right atrium (0.2 ml . kg(-1). min(-1) for 10 min). As a group (n = 59), PC activi ty increased from a baseline of 0.4 +/- 0.1 to a peak of 1.7 +/- 0.2 i mpulses/s during the period from 1 min before to 2 min after the termi nation of PAE induction. In PCs initially stimulated by PAE induction, PAE was repeated after the intervening treatment (iv) with saline (n = 9), ibuprofen (a cyclooxygenase ase inhibitor; n = 11), or dimethylt hiourea (a . OH scavenger; n = 12); The responses of PCs to PAE were n ot altered by saline vehicle but were abolished by ibuprofen and signi ficantly attenuated by dimethylthiourea. Although hyperinflation of th e lungs reversed the PAE-induced bronchomotor responses, it did not re verse the stimulation of PCs (n = 8). These results suggest that 1) cy clooxygenase products are necessary for the stimulation of PCs by PAE, whereas changes in lung mechanics are not, and 2) the functional impo rtance of cyclooxygenase products may be mediated in part through the formation of . OH.