ROLE OF C FIBERS IN PHYSIOLOGICAL-RESPONSES TO OZONE IN RATS

Citation
M. Jimba et al., ROLE OF C FIBERS IN PHYSIOLOGICAL-RESPONSES TO OZONE IN RATS, Journal of applied physiology, 78(5), 1995, pp. 1757-1763
Citations number
47
Categorie Soggetti
Physiology
ISSN journal
87507587
Volume
78
Issue
5
Year of publication
1995
Pages
1757 - 1763
Database
ISI
SICI code
8750-7587(1995)78:5<1757:ROCFIP>2.0.ZU;2-2
Abstract
The purpose of this study was to evaluate the role of C fibers in airw ay responsiveness after exposure to ozone (O-3) in rats. The role of C fibers in the decreases in heart rate (HR) and core body temperature (T-c) that occur after inhalation of O-3 was also examined. Neonatal r ats were treated with capsaicin (Cap) or the vehicle used to dissolve capsaicin (Veh). Cap has been shown to cause permanent destruction of C fibers. When they reached adulthood, conscious minimally restrained rats were exposed to 2 ppm O-3 or to air for 3 h. Two hours after the cessation of exposure, rats were anesthetized and instrumented for the measurement of pulmonary mechanics and airway responsiveness to inhal ed aerosolized methacholine. O-3 had no effect on baseline pulmonary c onductance (GL) in either Veh or Cap rats but did cause a decrease in dynamic compliance (Cdyn) in Cap rats (P < 0.05). In Cap rats, O-3 exp osure caused a marked increase in airway responsiveness; the doses of inhaled aerosolized methacholine required to decrease GL and Cdyn by 5 0% were 6.5-fold and 9.8-fold lower in O-3-compared with air-exposed r ats (P < 0.005). In contrast, in Veh rats, O-3 did not alter responsiv eness. During O-3 exposure, there was a profound, almost 50%, decrease in HR as measured with implanted electrodes. A decrease in T-c (measu red with a rectal probe) of similar to 2.5 degrees C also occurred dur ing O-3 exposure. There was no significant effect of Cap pretreatment on the magnitude of these O-3-induced changes in HR and T-c. Our resul ts are consistent with the hypothesis that C fibers act to inhibit the development of hyperresponsiveness elicited by O-3 inhalation but do not contribute to Os-induced changes in HR or T-c.