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POTENTIATION OF PULMONARY REFLEX RESPONSE TO CAPSAICIN 24 HOURS FOLLOWING WHOLE-BODY ACROLEIN EXPOSURE IS MEDIATED BY TRPV1
HAZARI, M. S., W. H. ROWAN, D. W. WINSETT, A. D. LEDBETTER, N. HAYKAL-COATES, W. P. WATKINSON, AND D. L. COSTA. POTENTIATION OF PULMONARY REFLEX RESPONSE TO CAPSAICIN 24 HOURS FOLLOWING WHOLE-BODY ACROLEIN EXPOSURE IS MEDIATED BY TRPV1. Respiratory Physiology and Neurobiology. Elsevier BV, AMSTERDAM, Netherlands, 160(2):160-71, (2008).
These experiments were designed to determine the effects of whole-body acrolein exposure and pulmonary C-fiber sensitization post-acrolein.
Pulmonary C-fibers are stimulated by irritant air pollutants producing apnea, bronchospasm, and decrease in HR. C-fiber chemoreflex activation is mediated by TRPV1 and release of substance P. While acrolein has been shown to stimulate C-fibers, the persistence of acrolein effects and the role of C-fibers in these responses are unknown. These experiments were designed to determine the effects of whole-body acrolein exposure and pulmonary C-fiber sensitization post-acrolein. Rats were exposed to either air or 3ppm acrolein for 3 hours while ventilatory function and HR were measured; 1 day later, response to capsaicin-challenge was measured in anesthetized rats. During acrolein exposure, rats experienced apnea and decrease in HR, which was not affected by either TRPV1 antagonist, or NK1R antagonist pretreatment. 24hrs later, capsaicin caused apnea and bronchoconstriction in control rats, which was potentiated by acrolein exposure. Pretreatment with TRPV1 antagonist or NK1R antagonist prevented potentiation of apneic response and bronchoconstriction 24hrs post-exposure. These data suggest that sensitization of pulmonary C-fibers by acrolein, but not direct activation, involves TRPV1 and release of SP.