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机构地区:[1]第一军医大学南方医院普外科
出 处:《中国应用生理学杂志》1998年第2期154-156,共3页Chinese Journal of Applied Physiology
摘 要:目的:观察失血性休克后血浆IL-1活性的变化及其与肠源性内毒素血症的关系。方法:复制容量控制失血性休克及肠源性内毒素血症模型,改良LAF法及显色基质偶氮法检测IL-1及ET。结果:普通SD大鼠30%失血后2~3h及6~10h血浆IL-1活性升高,3h后ET水平显著升高;失血前胃内灌注双岐杆菌或失血后静注rBPI,大鼠血浆ET水平无明显升高,IL-1活性第1峰仍然存在,但第2峰消失。无菌SD大鼠10%失血、灌注LPS后1h血浆ET水平升高,2h后IL-1活性升高。结论:失血性休克后IL-1活性呈双峰型升高,第1峰与内毒素无关,第2峰为内毒素刺激峰。Objective: To observe alterations of IL 1 activity and its relation with enterogenous endotoxemia in hemorrhagic shock. Method: Plasma IL 1 activity and endotoxin (ET) level were tested with modified LAF method and limulus test respectively in reproducing volume controlled hemorrhagic shock and enterogenous endotoxemia model. Result: There were significant increases in plasma IL 1 activities during 2~3 h and 6~10 h, and in plasma ET level during 3~10 h in conventional SD rats posthemorrhagic shock. After oral administration of bifidobacteria prehemorrhage or introvenous injection of rBPI posthemorrhage, there was a marked increase in plasma IL 1 activity during 2~3 h posthemorrhage, no remarkable change was found in plasma ET level during 3~10 h, or plasma IL 1 activity during 6~10 h posthemorrhage. While there were significant increases in plasma ET level at 1h and in plasma IL 1 activity at 2 h in endotoxemia rats after lipopolysaccharide (LPS) administration. Conclusion: Plasma IL 1 activity rise as a two peak style post hemorrhagic shock. The first peak (2~3 h posthemorrhage) has no relation with ET. While the second peak (6~10 h posthemorrhage) is caused mainly by ET which is derived mainly from guts.
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