Hershenson M B, Garland A, Kelleher M D, Zimmermann A, Hernandez C, Solway J
Department of Pediatrics, University of Chicago, Illinois.
Am Rev Respir Dis. 1992 Nov;146(5 Pt 1):1294-300. doi: 10.1164/ajrccm/146.5_Pt_1.1294.
We recently found that exposure of 21-day-old rats to hyperoxia (> 95% O2 for 8 days) significantly increased in vivo airway cholinergic responsiveness and that O2 exposure also increased airway epithelial and smooth muscle layer thicknesses in a separate cohort of animals. There was substantial variation in the magnitude of both the functional and structural responses to hyperoxia. The present study was designed to test whether the magnitude of O2-induced airway remodeling could account for individual differences in airway responsiveness after O2 exposure, as well as for the difference in responsiveness between air- and O2-exposed animals. We assessed in vivo airway responsiveness to aerosolized acetylcholine (ACh) and airway architecture in 14 O2- and 5 air-exposed, immature rats. Total respiratory system resistance was determined using a plethysmographic method. The mean thicknesses and fractional areas of the airway epithelial and smooth muscle layers were determined by contour tracing using a digitizing pad and microcomputer. Both the small (circumference < 1,000 microns) and central (circumference 1,000 to 4,000 microns) airways were studied. For O2-exposed rats, individual values of EC200 ACh correlated negatively with small airway smooth muscle layer thickness (r = -0.59, p < 0.05; ANOVA), small airway smooth muscle layer fractional area (r = -0.75, p < 0.01), small airway epithelial thickness (r = -0.54, p < 0.05), small airway epithelial fractional area (r = -0.69, p < 0.01), and central airway smooth muscle layer thickness (r = -0.53, p < 0.05). When both air- and O2-exposed animals were considered, EC200 ACh correlated negatively with all eight parameters of airway layer thickness and fractional area.(ABSTRACT TRUNCATED AT 250 WORDS)
我们最近发现，将21日龄大鼠暴露于高氧环境（> 95% O₂，持续8天）会显著增加体内气道胆碱能反应性，并且在另一组动物中，氧气暴露还会增加气道上皮和平滑肌层厚度。对高氧的功能和结构反应的程度存在很大差异。本研究旨在测试氧气诱导的气道重塑程度是否可以解释氧气暴露后气道反应性的个体差异，以及空气暴露和氧气暴露动物之间反应性的差异。我们评估了14只暴露于氧气和5只暴露于空气的未成熟大鼠的体内气道对雾化乙酰胆碱（ACh）的反应性和气道结构。使用体积描记法测定总呼吸系统阻力。通过使用数字化仪和微型计算机进行轮廓追踪来确定气道上皮和平滑肌层的平均厚度和面积分数。研究了小气道（周长< 1000微米）和中央气道（周长1000至4000微米）。对于暴露于氧气的大鼠，ACh的EC200个体值与小气道平滑肌层厚度（r = -0.59，p < 0.05；方差分析）、小气道平滑肌层面积分数（r = -0.75，p < 0.01）、小气道上皮厚度（r = -0.54，p < 0.05）、小气道上皮面积分数（r = -0.69，p < 0.01）以及中央气道平滑肌层厚度（r = -0.53，p < 0.05）呈负相关。当同时考虑空气暴露和氧气暴露的动物时，ACh的EC200与气道层厚度和面积分数的所有八个参数呈负相关。（摘要截断于250字）
