Takata S, Aizawa H, Inoue H, Koto H, Hara N
Research Institute for Diseases of the Chest, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Lung. 1995;173(1):47-56. doi: 10.1007/BF00167600.
We examined the effect of exposure to ozone on the epithelium-dependent relaxation (EpDR) of bronchioles evoked by electrical field stimulation (EFS) in a feline model with hyperresponsive airways induced by exposure to ozone. Airway responsiveness was assessed by measuring the increases in total pulmonary resistance (RL) produced by aerosolized acetylcholine (ACh) in vivo. Airway responsiveness was also measured in vitro in dissected bronchiolar ring preparations. Exposure to ozone (3 ppm, 2h) significantly increased the airway responsiveness in vivo. The concentration of ACh required increasing RL to 200% of the baseline value, decreased from 1.97 mg/ml (GSEM 1.94) to 0.12 mg/ml (GSEM 1.77, p < 0.01) after exposure to ozone. EFS evoked atropine-, guanethidine-, and tetrodotoxin-resistant relaxations in the control bronchiolar rings precontracted by 5-hydroxytryptamine. Such relaxation was significantly suppressed by the mechanical denudation of epithelium, confirming that it was epithelium dependent. The amplitude of the EpDR was significantly suppressed in the animals exposed to ozone. These results suggest that EpDR is present in cats, and that its inhibition may contribute to the development of airway hyperresponsiveness.
我们在一个通过暴露于臭氧诱导气道高反应性的猫模型中,研究了暴露于臭氧对电场刺激(EFS)诱发的细支气管上皮依赖性舒张(EpDR)的影响。通过测量雾化乙酰胆碱(ACh)在体内引起的总肺阻力(RL)增加来评估气道反应性。还在离体细支气管环制备物中体外测量气道反应性。暴露于臭氧(3 ppm,2小时)显著增加了体内气道反应性。使RL增加至基线值200%所需的ACh浓度,在暴露于臭氧后从1.97 mg/ml(几何标准误1.94)降至0.12 mg/ml(几何标准误1.77,p<0.01)。在由5-羟色胺预收缩的对照细支气管环中,EFS诱发了对阿托品、胍乙啶和河豚毒素抵抗的舒张。这种舒张被上皮的机械剥脱显著抑制,证实其为上皮依赖性。在暴露于臭氧的动物中,EpDR的幅度显著受到抑制。这些结果表明猫存在EpDR,并且其抑制可能促成气道高反应性的发展。