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[白细胞介素-1在出血性休克中与内毒素相关的调节机制]

[Modulation mechanism of IL-1 in hemorrhagic shock in relation to endotoxin].

作者信息

Shi H P, Miao M Y, Qin L P, Gao H, Xu R B

机构信息

Department of General Surgery, South Hospital, First Military Medical University, Guangzhou.

出版信息

Sheng Li Xue Bao. 1997 Apr;49(2):173-7.

PMID:9812853
Abstract

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.

摘要

在内毒素(ET)相关的白细胞介素-1(IL-1)调节机制方面,对失血性休克大鼠进行了研究。结果发现,在失血性休克后4小时内,SD大鼠的ET和IL-1均显著增加,且IL-1的增加早于ET。而在无菌条件下饲养的SD大鼠,无论是否用乳果糖或抗ET进行预处理,IL-1均明显增加,但ET无明显变化。普通休克大鼠回输失血量后5天内,IL-1和ET呈平行变化。当休克大鼠用乳果糖或抗ET治疗时,与对照组相比,IL-1和ET均显著降低。从上述观察结果表明,ET在失血性休克早期不是增强IL-1活性的重要因素,但在失血性休克后期确实有助于IL-1活性的增加。失血性休克时ET主要来源于肠道。

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