实验性肾炎中肾皮质内血小板活化因子的水平和可能来源

The level and potential origin of platelet activating factor in the renal cortex in experimental glomerulonephritis

用大鼠复制加速型抗肾小球基底膜（ＧＢＭ）肾炎模型，分为４组：肾毒血清对照组、肾毒血清＋眼镜蛇毒因子（ＣＶＦ）组，肾毒血清＋羊抗大鼠血小板血清（ＡＰＳ）组、肾毒血清＋全身γ线辐射（ＴγＩ）组。各组大鼠在注射兔抗大鼠ＧＢＭ血清后２４ｈ未处死，结果肾毒血清对照组大鼠肾皮质内ＰＡＦ含量显著升高，而耗尽补体的肾毒血清＋ＣＶＦ组、耗尽血小板的肾毒血清＋ＡＰＳ组和耗尽白细胞的肾毒血清＋ＴγＩ组大鼠肾皮质内ＰＡＦ含量显著低于肾毒血清对照组（Ｐ＜０．０１），正常大鼠肾皮质内未测得ＰＡＦ．因此，本实验表明：大鼠加速型抗ＧＢＭ肾小球肾炎肾皮质内ＰＡＦ含量显著升高，后者部分来源于存在于肾内的血小板、白细胞，并与补体的激活相关。

Rats for experiment were divided into four groups:control group,nephrotoxic se-rum + CVF (cobra venum factor)group, nephrotoxic neruephrotoxic serum+APS(goat anti-rat platelet immune se-rum)group and nephrotoxic serum + Tγ I(total γ-ray irradiation)group.All the rats vere injectedwith the nep nephrotoxic serum. 24 hours Iater,all the rats were killed and platelet a ctivating factor(PAF)in the renal cortex was detected. The results showed that in the control group,the amountof PAF in renal cortex was enhanced significantly, whereas in the other ther groups PAF wereall reduced significantly. In normal rats the amount of PAF in the renal cortex couldn·t been found.These results suggested that(1)The amount of PAF in renal cortex in the rat model of acceleratedanti-GBM(glomerular basement membrane) glomerulonephritis significantly enhaneed;(2)Theincreased amo unt o f PAF in the renal cortex is partially originated from the infiltratingplatelets,leuco cytes and related with the comp lement mediated mechanism.