摘要
目的:探讨腹腔高压动物模型肝脏的继发改变.方法:实验兔30只,分为ACS1组、ACS2组、对照组,每组10只.水囊法制作ACS动物模型,调整腹腔压力维持在20-25 cmH2O.ACS1组观察时限3 d,ACS2组观察时限7 d,完成观察时间后,抽血行肝脏功能检查,即刻处死各组实验动物,完整取出兔肝脏,固定后在生物光学显微镜下观察.结果:与对照组相比:ACS1组谷丙转氨酶(alanine transaminase,ALT)、谷草转氨酶(aspartate transaminase,AST)、碱性磷酸酶(alkaline phosphatase,AKP)显著升高(P<0.05,P<0.01,P<0.01),γ-谷氨酰转肽酶(γ-glutamyl transpeptidase,GGT)无明显改变(P>0.05);ACS2组ALT、AST、AKP、GGT显著升高(P<0.01,P<0.01,P<0.01,P<0.05),而且ALT、AST、AKP显著高于ACS1组(P<0.01,P<0.05,P<0.01),GGT无明显升高(P>0.05).病理变化:ACS1组:肝脏结构存在,可见正常肝小叶,可见中央静脉、肝索、肝窦及汇管区.肝细胞气球样变性,脂褐素沉积,部分血管内布满淡红染无结构物质,汇管区少许炎细胞浸润.ACS2组:肝脏结构存在,肝细胞弥漫重度气球样变性,细胞增生,大片脂褐素沉积,间质轻度纤维化,汇管区血管扩张、充血,胆管增生,炎细胞浸润,肝细胞内淤胆.结论:腹腔高压可引起肝脏出现明显的酶学和细胞学变化,随着持续时间的延长,损害加重.
AIM： To analyze the secondary liver changes in ananimal model of intra-abdominal hypertension.METHODS： Thirty rabbits were equally divided into an Abdominal compartment syndrome 1（ACS1） group, an ACS2 group and a control group. ACS was induced in animals by the water sac method, and the abdominal cavity pressure was adjusted at 20-25 cmH2 O. The observation time was 3 d for the ACS1 group was 3 d, and 7 d for the ACS2 group. After observation, liver function was detected. Animals were then sacrificed to remove the rabbit liver tissue for pathological examination.RESULTS： Compared with the control group, alanine transaminase（ALT）, aspartate transaminase（AST）, and alkaline phosphatase（AKP） in the ACS1 group were significantly（P 0.05, P 0.01, P 0.01）, and γ-glutamyl transpeptidase（GGT） showed no significant change（P 0.05）. ALT, AST, AKP, and GGT were significantly higher in the ACS2 group than in the control group（P 0.01, P 0.01, P 0.01, P 0.05）. ALT, AST, and AKP were significantly higher in the ACS2 group than in the ACS1 group（P 0.01, P 0.05, P 0.01）, although GGT showed no significant difference（P 0.05）. In the ACS1 group, hepatic lobule, hepatic cords, central vein, hepatic sinus and portal area were all visible; hepatocytes showed ballooning degeneration; there was lipofuscin deposit; part of blood vessels were filled with pink dye materials; and some inflammatory cells appeared in the portal area. In the ACS2 group, hepatocytes showed severe ballooning degeneration; cells proliferated significantly; there were lots of lipofuscin deposit; mild fibrosis occurred;vasodilation and congestion appeared in the portal area; and there was inflammatory cell infiltration.CONCLUSION： Intra-abdominal hypertension can cause significant liver enzymological and cytological changes, and with the extension of duration, the damage is aggravating.
出处
《世界华人消化杂志》
CAS
2016年第9期1393-1397,共5页
World Chinese Journal of Digestology
基金
山西大同科技攻关基金资助项目
No.201497~~
关键词
腹腔高压
动物模型
肝酶
病理检查
Intra-abdominal hypertension
Animal model
Liver enzyme
Pathology
