盲肠穿孔所致幼鼠急性腹膜炎模型的建立  

Establishment the infant mouse model of acute peritonitis caused by cecal ligation perforation

作　　者：黄薇[1] 李毅平[1] 汪健[1] 

机构地区：[1]苏州大学附属儿童医院新生儿外科,江苏苏州215003

出　　处：《苏州大学学报（医学版）》2012年第2期237-240,共4页Suzhou University Journal of Medical Science

摘　　要：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 an infant mouse model of polymicrobial acute peritonitis, which is similar to clinical syndrome. Methods we established a surgical connection between the cecum and the peritoneum （by placing a sterile 18-gauge silicon tube across the cecum）which allowed the exit of in- testinal bacteria to the peritoneal cavity. The general situation and the time of death were recorded. One week later, the mice were killed and abdominal fluid was collected for bacteria culture in Luria-Bertani agar. The livers, spleens and kidneys were dissected and generated for pathological examination. Results The experiment groups showed typical clinical syndrome of peritonitis. The 48-hour mortality rate was 50% , the weight of mice decreased progressively. Abdominal fluid cultures were positive. Moreover, the pathological examination of liver and adipose tissue around the kidney revealed inflammatory cells infiltra- tion. Conclusions The infant mouse model of polymicrobial peritonitis is constructed successfully, pro- viding a useful tool to develop new diagnostic methods and therapeutic interventions.

关 键 词：盲肠穿孔 急性腹膜炎 幼鼠 

分 类 号：R656.41[医药卫生—外科学]