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  

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

作　　者：石汉平[1] 缪明永[2] 秦路平[3] 高瀚[4] 徐仁宝[5] 

机构地区：[1]第一军医大学南方医院普外科,广州510515 [2]第二军医大学生化教研室,上海200433 [3]第二军医大学生药教研室,上海200433 [4]第二军医大学长征医院普外科,上海200002 [5]第二军医大学病理生理教研室,上海200433

出　　处：《生理学报》1997年第2期173-177,共5页Acta Physiologica Sinica

摘　　要：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，血浆IL－1活性及ET水平均明显降低。上述结果提示，失血性休克早期血浆IL－1活性升高与内毒素刺激无关，但后期IL－1活性升高与内毒素相关，内毒素主要来源于肠道。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.

关 键 词：失血性休克 内毒素 白细胞介素I 

分 类 号：R605.971[医药卫生—急诊医学]