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二氧化硫与麻醉兔冷诱导支气管痉挛之间的相互作用。

Interaction between SO2 and cold-induced bronchospasm in anesthetized rabbits.

作者信息

Barthélemy P, Badier M, Jammes Y

机构信息

Laboratoire de Médecine Expérimentale, GS 15 (CNRS), Faculté de Médecine, Marseille, France.

出版信息

Respir Physiol. 1988 Jan;71(1):1-10. doi: 10.1016/0034-5687(88)90110-7.

Abstract

In anesthetized, paralyzed and artificially ventilated rabbits, reflex changes in lung resistance induced by cooling the inspired air from 38 to 15 degrees C were studied before and after 45 min periods of SO2 exposure at two different concentrations (0.5 or 5 ppm). Both concentrations of SO2 induced significant increase in RL in intact animals (+16% and +50%, respectively). The effect of 5 ppm SO2 persisted after vagotomy. The cold-induced bronchospasm was halved after exposure to 0.5 ppm SO2 and was no longer significant after exposure to 5 ppm SO2. In both cases, RL recovered to control values 40 min after the end of SO2 exposure and then, the magnitude of cold-induced bronchospasm also recovered. The reflex bronchoconstrictor response to phenyldiguanide (PDG) i.v. disappeared after exposure to 5 ppm SO2. However, the bronchomotor response to histamine i.v., which involved both reflex and direct actions on airway smooth muscle, was not altered. These results show that (1) prolonged increase in RL measured after SO2 exposure does not result from a vagal reflex; (2) the cold-induced bronchospasm, as well as the bronchomotor response to PDG, are reduced or suppressed during the period where the effect of SO2 persisted. This suggests that 45 min exposure to SO2 induces transient alterations in tracheobronchial wall, which reduce the accessibility to nervous receptors in the airways.

摘要

在麻醉、麻痹并进行人工通气的家兔中,研究了在两种不同浓度(0.5或5 ppm)的二氧化硫暴露45分钟前后,将吸入空气从38℃冷却至15℃所诱发的肺阻力反射性变化。两种浓度的二氧化硫均使完整动物的肺阻力显著增加(分别增加16%和50%)。5 ppm二氧化硫的作用在迷走神经切断后依然存在。暴露于0.5 ppm二氧化硫后,冷诱导的支气管痉挛减轻了一半,暴露于5 ppm二氧化硫后则不再显著。在这两种情况下,二氧化硫暴露结束40分钟后,肺阻力恢复到对照值,随后,冷诱导支气管痉挛的程度也恢复了。静脉注射苯基双胍(PDG)所引起的反射性支气管收缩反应在暴露于5 ppm二氧化硫后消失。然而,静脉注射组胺所引起的支气管运动反应,该反应涉及对气道平滑肌的反射和直接作用,并未改变。这些结果表明:(1)二氧化硫暴露后测得的肺阻力长时间增加并非由迷走神经反射引起;(2)在二氧化硫作用持续期间,冷诱导的支气管痉挛以及对PDG的支气管运动反应均减弱或受到抑制。这表明,暴露于二氧化硫45分钟会引起气管支气管壁的短暂改变,从而降低气道中神经受体的可及性。

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