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Institute of Physiology, School of Medicine and Life Science, National Yang-Ming University, Taipei, Taiwan 11221, Republic of China
Received 12 August 1996; accepted in final form 29 October 1996.
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
1
for 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.
lung vagal sensory receptors; microembolism; reflex tachypnea; ibuprofen; dimethylthiourea; cyclooxygenase system; hydroxyl radical
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