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目的：观察烟雾吸入伤大鼠肺上皮细胞通透性的变化及ＢＮ５０７３９ 与氢溴酸山莨菪碱的防治作用，并探讨其机制。方法：常规方法复制大鼠吸入伤模型，分别采用气相色谱法、９９ Ｔｃ－ ＤＴＰＡ 法（ 或伊文斯兰荧光法） 、微量酸滴定法、ＴＢＡ 比色法及放射免疫分析法，测定致伤烟雾中烃类物质的含量、肺上皮细胞通透性、ＰＬＡ２ 活性、脂质过氧化物ＭＤＡ 及ｃＡＭＰ的含量。结果：烟雾吸入伤后，大鼠肺上皮细胞通透性明显增大，肺组织ＰＬＡ２ 活性增强、ＭＤＡ 含量及致伤烟雾中烃类物质明显升高，而肺组织ｃＡＭＰ水平显著降低。ＢＮ５０７３９ 能剂量依赖性地降低吸入伤肺上皮细胞通透性，并抑制肺组织ＰＬＡ２ 活性，降低ＭＤＡ 含量，升高ｃＡＭＰ水平；氢溴酸山莨菪碱具有类似作用。结论：烟雾吸入伤后，大鼠肺上皮细胞通透性明显升高，ＢＮ５０７３９ 及氢溴酸山莨菪碱对吸入性肺损伤有一定防治作用，其机制与抑制肺组织ＰＬＡ２ 活性及脂质过氧化反应，升高ｃＡＭＰ含量有关
Objective: To observe the changes of pulmonary epithelial cells permeability induced by smoke inhalation injury and the preventive and therapeutic effects of BN50739 and anisodamine hydrobromide, and to explore its mechanism. Methods: The rat model of inhalation injury was established by conventional method. Gas chromatography, 99 Tc-DTPA (or Evans blue fluorescence), trace acid titration, TBA colorimetric assay and radioimmunoassay Medium hydrocarbon content, pulmonary epithelial cell permeability, PLA2 activity, lipid peroxidation MDA and cAMP content. Results: After inhalation of smoke, the permeability of lung epithelial cells in rats increased significantly, the activity of PLA2 in lung tissue increased, the content of MDA and the content of hydrocarbon in injured smoke increased significantly, while the level of cAMP in lung tissue decreased significantly. BN50739 could reduce the permeability of injured lung epithelial cells in a dose-dependent manner, inhibit PLA2 activity in lung tissue, decrease MDA content and increase cAMP level; CONCLUSION: After inhalation of smoke, the permeability of lung epithelial cells in rats is obviously increased. BN50739 and anisodamine hydrobromide have some preventive and therapeutic effects on inhalation lung injury. The mechanism is related to inhibition of PLA2 activity and lipid peroxidation Response, increased cAMP content