内毒素和过氧化氢对肺血管内皮细胞的损伤作用

Destructive Effects of Endotoxin and H_2O_2 on Pulmonary Vascular Endothelial Cells

观察内毒素、中性粒细胞弹性蛋白酶、中性粒细胞组织蛋白酶Ｇ和过氧化氢对肺血管内皮细胞释放５１Ｃｒ的影响，结果表明，体外培养的肺动脉内皮细胞经５１Ｃｒ标记后，内毒素和Ｈ２Ｏ２可使内皮细胞释放５１Ｃｒ明显增多；中性粒细胞弹性蛋白酶和组织蛋白酶的作用不明显。内毒素和Ｈ２Ｏ２增加内皮细胞内之５１Ｃｒ的释放，表明内皮细胞受到了损伤。

The effect of endotoxin(50ng/ml).human neutrophil elastase(SU/ml),human neutrophil cathepsin-G(30ug/ml) and H2O2(3umol/ml) on 51Cr-release from 51Cr labeled pulmonary arterial endothelial cells were investigated.Results showed that endotoxin and H2O2 significantly increased the 51Cr release from 51Cr labeled pulmonary arterial endothelial cells in vitro.The cpm of 51Cr in supernatant of endotoxin group and H2O2 group were 241.6±9.7(x±sx,n=12) and 280.5±22.9(x=11) respectively,compared with the cpm 135.3±6.4 (n=7) of control group both of them P<0.01,human neutrophil elastase(HNE) and cathepsin-G(C-G) showed no significant effect on 51Cr release from 51Cr labeled pulmonary arterial endothelial calls.The cpm in the supernatant of HNE group and C-G group were 133.1±3.9(n=8) and 137.5±5.3(n=11) respectively.It suggested that endotoxin and H2O2 showed destructive effect on pulmonary arterial endothelial cells.