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目的建立一种稳定、符合临床小儿消化道穿孔所致多种细菌性急性腹膜炎的模型。方法在3～4周龄BALB/c小鼠盲肠壁置入一个两端开放的18号无菌硅管,使得肠道内的细菌进入腹腔,观察实验小鼠每日情况,并记录体质量变化及死亡时间。1周后处死存活下来的小鼠,观察其腹腔内脏器外观改变情况,收集腹腔灌洗液做细菌培养,观察肝、脾、肾组织切片中炎症细胞的浸润情况。结果实验组小鼠均表现出细菌性腹膜炎征象,48 h死亡率高达50%,未死亡小鼠的体质量进行性下降,腹腔灌洗液细菌培养呈现阳性,病理切片显示肝实质、肾周围脂肪组织内有不同程度的炎症细胞浸润。结论幼鼠盲肠穿孔所致急性腹膜炎模型建立成功,这为探索小儿急性腹膜炎的发病机制和治疗方法奠定了基础。
Objective To establish a stable, consistent with clinical pediatric gastrointestinal perforation caused by a variety of bacterial acute peritonitis model. Methods A sterile silicone tube with two open ends 18 was placed in the cecal wall of BALB / c mice aged 3 to 4 weeks. The bacteria in the intestine were allowed to enter the abdominal cavity. The daily condition of the mice was observed. The changes of body weight and Death time. After 1 week, the surviving mice were sacrificed to observe the changes of their visceral organs. The peritoneal lavage fluid was collected for bacterial culture. The infiltration of inflammatory cells in liver, spleen and kidney tissue sections was observed. Results The mice in the experimental group showed signs of bacterial peritonitis with a mortality rate of up to 50% at 48 h. The body weight of mice that did not die decreased progressively. The bacterial culture in peritoneal lavage fluid was positive. The pathological sections showed hepatic parenchyma, perirenal fat There are varying degrees of inflammatory cell infiltration within the tissue. Conclusion The model of acute peritonitis caused by cecal perforation in young rats was successfully established, which laid the foundation for exploring the pathogenesis and treatment of acute peritonitis in infants.