Mechanisms of stimulation of vagal pulmonary C fibers by pulmonary air embolism in dogs

Abstract

Chen, H. F., B. P. Lee, and Y. R. Kou. Mechanisms of stimulation of vagal pulmonary C fibers by pulmonary air embolism in dogs. J. Appl. Physiol. 82(3): 765–771, 1997.—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 PCs in 51 anesthetized, open-chest, and artificially ventilated dogs. Fifty of 59 PCs were stimulated by infusion of air into the right atrium (0.2 ml ⋅ kg−1 ⋅ min−1for 10 min). As a group ( n = 59), PC activity increased from a baseline of 0.4 ± 0.1 to a peak of 1.7 ± 0.2 impulses/s during the period from 1 min before to 2 min after the termination 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 inhibitor; n = 11), or dimethylthiourea (a ⋅ OH scavenger; n = 12). The responses of PCs to PAE were not altered by saline vehicle but were abolished by ibuprofen and significantly attenuated by dimethylthiourea. Although hyperinflation of the lungs reversed the PAE-induced bronchomotor responses, it did not reverse the stimulation of PCs ( n= 8). These results suggest that 1) cyclooxygenase products are necessary for the stimulation of PCs by PAE, whereas changes in lung mechanics are not, and 2) the functional importance of cyclooxygenase products may be mediated in part through the formation of ⋅ OH.