Jimba M, Skornik W A, Killingsworth C R, Long N C, Brain J D, Shore S A
Department of Environmental Health, Harvard School of Public Health, Boston, Massachusetts 02115, USA.
J Appl Physiol (1985). 1995 May;78(5):1757-63. doi: 10.1152/jappl.1995.78.5.1757.
The purpose of this study was to evaluate the role of C fibers in airway responsiveness after exposure to ozone (O3) in rats. The role of C fibers in the decreases in heart rate (HR) and core body temperature (Tc) that occur after inhalation of O3 was also examined. Neonatal rats 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 O3 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 inhaled aerosolized methacholine. O3 had no effect on baseline pulmonary conductance (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, O3 exposure caused a marked increase in airway responsiveness; the doses of inhaled aerosolized methacholine required to decrease GL and Cdyn by 50% were 6.5-fold and 9.8-fold lower in O3-compared with air-exposed rats (P < 0.005). In contrast, in Veh rats, O3 did not alter responsiveness. During O3 exposure, there was a profound, almost 50%, decrease in HR as measured with implanted electrodes. A decrease in Tc (measured with a rectal probe) of approximately 2.5 degrees C also occurred during O3 exposure. There was no significant effect of Cap pretreatment on the magnitude of these O3-induced changes in HR and Tc. Our results are consistent with the hypothesis that C fibers act to inhibit the development of hyperresponsiveness elicited by O3 inhalation but do not contribute to O3-induced changes in HR or Tc.
本研究的目的是评估C纤维在大鼠暴露于臭氧(O3)后气道反应性中的作用。还研究了C纤维在吸入O3后心率(HR)和核心体温(Tc)下降中的作用。新生大鼠用辣椒素(Cap)或用于溶解辣椒素的赋形剂(Veh)处理。已证明Cap会导致C纤维永久性破坏。成年后,将清醒的轻度束缚大鼠暴露于2 ppm O3或空气中3小时。暴露停止后两小时,将大鼠麻醉并安装仪器以测量肺力学和气道对吸入雾化乙酰甲胆碱的反应性。O3对Veh或Cap大鼠的基线肺电导(GL)均无影响,但确实导致Cap大鼠的动态顺应性(Cdyn)下降(P <0.05)。在Cap大鼠中,O3暴露导致气道反应性显著增加;与空气暴露的大鼠相比,使GL和Cdyn降低50%所需的吸入雾化乙酰甲胆碱剂量在O3暴露的大鼠中低6.5倍和9.8倍(P <0.005)。相反,在Veh大鼠中,O3不会改变反应性。在O3暴露期间,用植入电极测量的HR显著下降,几乎下降了50%。在O3暴露期间,直肠探头测量的Tc也下降了约2.5摄氏度。Cap预处理对这些O3诱导的HR和Tc变化的幅度没有显著影响。我们的结果与以下假设一致,即C纤维起到抑制吸入O3引起的高反应性发展的作用,但对O3引起的HR或Tc变化没有贡献。