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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，内毒素主要来源于肠道
Objective: To observe the changes of plasma IL-1 activity after hemorrhagic shock and its relationship with enterogenous endotoxemia. Methods: Hemorrhagic shock and intestinal endotoxemia were induced by replication volume. IL-1 and ET were measured by modified LAF method and chromogenic matrix azo method. Results: The levels of plasma IL-1 in normal SD rats were increased at 2 ~ 3h and 6 ~ 10h after 30% blood loss, and increased significantly after 3h. After intragastric administration of Bifidobacterium before blood loss or rBPI after blood loss, rats Plasma ET levels did not increase significantly, the first peak of IL-1 activity still existed, but the second peak disappeared. After 10% blood loss of aseptic Sprague-Dawley rats, plasma ET level increased 1 hour after perfusion of LPS, and IL-1 activity increased after 2 hours. CONCLUSION: After hemorrhagic shock, the activity of IL-1 is bimodal, the first peak is not related to endotoxin, the second peak is endotoxin stimulation peak, endotoxin mainly comes from intestine