摘要
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。
AIM To obsesve the changes of pulmonary epithelial permeability after smoke inhalation injury(SII) in rats and the prophylactic effects of BN50739 and 654-2 on it and to expltore there action mechinsm.METHODS The model of SII in rats was made by routine method.Contents of hydrocarbons,pulmonary epithelial permeability,the activity of PLA 2, lipoperoxidates MDA level and the content of cAMP were determined with gas chromatography, 99 Tc-DTPA technique, micro-acid titration, thiobarbiluric acid spectrophotometer, and radioimmunoassay, respectively.RESULTS The permeability of pulmonary epithelia was enlarged, the activity of PLA 2 in lung tissues was enhanced,and the contents of MDA were increased obviously after SII in rats.However,the levels of cAMP in lung tissues were decreased. The contents of hydrocarbons were also elevated sharply during the period of injury. In addition,BN50739 inhibited the enlargement of pulmonary epithelial permeability, the enhancing of PLA 2 activity, and the increasement of MDA content, but elevated the level of cAMP dosedependently after SII in rats. 654-2 had the similar effects.CONCLUSION The pulmonary epithelial permeability enlarged greatly after SII in rats, BN50739 and 654-2 had some prophylactic effects on it, the mechanisms of which were related to the inhibition of PLA 2 activity, alleviation of lipoperoxidation damage, and the elevation of cAMP.
出处
《解放军药学学报》
CAS
1999年第3期1-3,共3页
Pharmaceutical Journal of Chinese People's Liberation Army
基金
国家自然科学基金
