失血性休克早期白细胞介素1活性升高的机制——内毒素与白细胞介素1

本文观察了失血性休克条件下大鼠白细胞介素１（ＩＬ－１）与内毒素的关系。结果表明：失血性休克早期血浆ＩＬ－１及ＥＴ均明显升高，前者升高在先；无菌大鼠失血性休克后ＩＬ－１活性也升高，但ＥＴ无明显变化；预先给大鼠口服乳果糖以清洁肠道，或静注内毒素抗体，休克后血浆ＩＬ－１活性仍然明显升高，而血浆ＥＴ无明显升高；大鼠失血后１ｈ将失血回输再灌注后５ｄ血浆ＩＬ－１与ＥＴ呈平行性变化，乳果糖或抗内毒素抗体治疗后，

MODULATION MECHANISM OF IL-1 IN HEMORRHAGIC SHOCK IN RELATION TO ENDOTOXIN

The modulation mechanism of IL-1 in relation to endotoxin (ET) was investigated in hemorrhangic shock rat. It was found that within 4 h after hemorrhagic shock, SD rat showed a significant increase in both ET and IL-1, the latter taking place earlier than the former. While SD rat reared in germ free condition showed an obvious increas in IL-1 but without marked change in ET, no matter whether the rats reared in different condition were pretreated with lactuolsc or anti-ET. Within 5 d after reinfusion of lost blood to the ordinary shock rat, IL-1 and ET changed in a parallel manner. When shock rats were treated with lactulose or anti-ET, both IL-1 and ET showed significant decrease as compared with the control. It is suggested from the above observation that ET is not an important factor in enhancing IL-1 activity in the early stage of hemorrhagic shock, but does contribute to the increased IL-1 activity in the later phase of hemorrhagic shock. The ET comes mainly from the gut in hemorrhagic state.