Mechanisms of stimulation of vagal pulmonary c-fibers by pulmonary
air embolism in dogs.
Chen, H. F., B. P. Lee, and Y. R. Kou.
Institute of Physiology, School of Medicine and Life Science,
National Yang-Ming University, Taipei, Taiwan 11221, Republic of
China
APStracts 3:0519A, 1996.
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 out of 59 PCs were stimulated by infusion of air into the
right atrium (0.2 ml/kg/min 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
following the termination of PAE induction. In PCs initially
stimulated by PAE induction, PAE was repeated following the
intervening treatment (iv) with saline (n = 9), ibuprofen (IBU; a
cyclooxygenase inhibitor; n = 11), or dimethylthiourea (DMTU; a _ OH
scavenger; n = 12). The responses of PCs to PAE were not altered by
saline vehicle, but were abolished by IBU and significantly
attenuated by DMTU. While 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.
Received 12 August 1996; accepted in final form 29 October 1996.
APS Manuscript Number A770-6.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 31 December 1996