Marthan R, Roux E, Savineau J P
Laboratoire de Physiologie Cellulaire Respiratoire, Université Bordeaux 2, France.
Cell Biol Toxicol. 1996 Dec;12(4-6):245-9. doi: 10.1007/BF00438153.
The aims of this work were (1) to determine the dose-response relationship between ex vivo exposure to oxidizing pollutants such as nitrogen dioxide (NO2), the aldehyde acrolein, and ozone (O3), and the reactivity to agonists in isolated human bronchial smooth muscle; and (2) to investigate the alterations in the cellular mechanisms of human airway smooth muscle contraction induced by such exposures. Experiments were performed in isolated human bronchi obtained at thoracotomy. Isometric contraction in response to a variety of agonists was compared between pollutant-exposed preparations and paired controls. Short exposures to NO2, acrolein, or O3 altered the subsequent airway smooth muscle responsiveness in a dose-dependent manner. The cellular mechanisms producing the airway hyperresponsiveness observed in vitro are shared by the three pollutants and include alterations in airway smooth muscle excitation-contraction coupling as well as indirect effects on neutral endopeptidase activity.
（1）确定离体暴露于氧化污染物（如二氧化氮（NO₂）、醛丙烯醛和臭氧（O₃））与离体人支气管平滑肌中激动剂反应性之间的剂量反应关系；（2）研究此类暴露引起的人气道平滑肌收缩细胞机制的改变。实验在开胸手术获取的离体人支气管中进行。比较了暴露于污染物的标本和配对对照对各种激动剂的等长收缩反应。短时间暴露于NO₂、丙烯醛或O₃会以剂量依赖的方式改变随后的气道平滑肌反应性。这三种污染物具有共同的体外观察到的引起气道高反应性的细胞机制，包括气道平滑肌兴奋 - 收缩偶联的改变以及对中性内肽酶活性的间接影响。
