内毒素腹腔内注射诱发小鼠肠套叠的实验研究

Intraperitoneal Injection of Lipopolysaccharide Induces Intussusception in Mice

报告了一种新型的内毒素肠套叠动物模型，并对其发病机理进行了初步探索。结果发现：给小鼠腹腔内注射内毒素，肠套叠诱发率为２３．８％，内毒素最佳剂量是１２ｍｇ／ｋｇ，肠套叠形成高峰时间在６～１２ｈ。内毒素使肠传递时间延长，一氧化氮合成酶抑制剂Ｌ－ＮＡＭＥ降低肠套叠诱发率。实验结果提示：内毒素可诱发肠套叠，其发病机理与肠动力紊乱有关。该动物模型可为研究肠套叠的病因，发病机理及治疗提供帮助。

Background:Intussusception is a common cause of intestinal obstruction in children.Its etiology is unclear,and research in this area has been hindered by the lack of a reproducible animal model.Methods:Lipopolysaccharide (LPS) was injected intraperitoneally in adult mice.At time points from two hours to eight days after the administration of LPS the animals were inspected for the presence of intussusception.Gastrointestinal transit was assessed by measuring the passage of charcoal in the small intestine.Transit index was defined as the ratio between the distance traveled by charcoal and the total length of the small intestine.Results:Intussusceptions were found in up to 23.8% of the LPS injected animals.The threshold for the LPS effect was at 4mg/kg,and incidence reached a plateau at 12mg/kg.The intrssusception incidence peaked at 6h after LPS injection and declined to zero after 15h.LPS (12mg/kg) reduced the transit index from (56.2±1.4)% to (37.7±2.1)%.The nitric oxide synthese inhibitor L NAME (20mg/kg) reduced the intussusception incidence from 23.8% to 3.8%.No pathological change was found in the intussuscepted bowels.Conclusions:LPS caused a high incidence of intussusception in mice,apparently by disturbing gastrointestinal motility.One putative mediator involved is NO.This model could be useful for studying the etiology and possible treatment of intussusception.