大白鼠出血性休克和多脏器功能障碍模型的建立

目的 :模拟多脏器功能障碍发病因素 ,建立大白鼠出血性休克和多脏器功能障碍模型。方法 :大白鼠经动脉放血 ,造成失血性休克模型 ,平均动脉血压降至 30～ 35mmHg,并维持 1h ,随后用 6 0 %自体血和 2倍血量的生理盐水从静脉回输 ,进行复苏 1h。大白鼠随机分成 3组 :正常对照组、假休克组 (不放血诱导休克 )、休克组 (放血诱导休克和复苏 )。结果 :复苏后 72h ,休克组的生存率降至 2 0 %。复苏后 18h器官病理取材 ,H E染色 ,光镜下显示 ,休克组大白鼠的心、肺、肾、肝组织出现不同程度水肿、变性、白细胞浸润、出血等。复苏后 18h ,检测CK、Cr、ALT、AST、ALKP指标 ,休克组明显升高 ,是正常值 3倍以上 ,提示心肌、肝脏、肾脏的损伤 ,与假休克组和正常大白鼠值比较 ,两者差异非常显著 (P <0 .0 1)。结论 :模拟临床休克致病因素 -出血性休克 -成功建立多脏器功能障碍大白鼠模型。

Establishment of Model of Hemorrhagic Shock and Multiple organ Dysfunction Syndrome in Rats

Objective: By imitating the injurious factors of multiple organ dysfunction syndrome (MODS), our aim was to establish the model of hemorrhagic shock and multiple organ dysfunction syndrome in rats. Methods:Rats were bled to maintain mean arterial pressure at 30 to 35 mmHg for 1 hour and then resuscitated with 60% shed blood and saline for 1 hour. The rats were divided into 3 groups: control group, shock group, and sham group. Results:The survival rate of shock group decreased to 20% 72 hours after resuscitation. Eighteen hours after resuscitation, pathologic examinations of organs showed pulmonary edema, leukocyte infiltration, and cellular degeneration in shock group. Creatine phosphokinase, transaminases and creatinine were increased significantly in shock group, indicating injury to heart, liver,and kidney. Compared with sham group and control group, the differences were significant (P<0.01). Conclusion:We successfully imitated the injurious factors of multiple organ dysfunction syndrome, and established the model of hemorrhagic shock and multiple organ dysfunction syndrome in rats.