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门静脉动脉化治疗大鼠急性肝衰竭

             

摘要

背景:部分门静脉动脉化可通过增加肝脏血供的方式减缓急性肝衰竭的发展.目的:观察部分门静脉动脉化对肝衰竭模型大鼠肝脏功能及病理学变化的影响.方法:将130只SD大鼠随机分为3组,动脉化组(n=50)切除左肾,以同种异体腹主动脉血管为移植材料,采用套入式缝合及袖套法建立门静脉动脉化模型,造模成功后一次性腹腔注射D-氨基半乳糖1300 mg/kg,诱导急性肝功能衰竭;肝衰竭组(n=50)切除左肾,游离门静脉,阻断门静脉16 min后开放,关闭腹腔后一次性腹腔注射 D-氨基半乳糖1300 mg/kg,诱导急性肝功能衰竭;对照组(n=30)切除左肾,阻断门静脉16 min后开放,关闭腹腔后一次性腹腔注射生理盐水1300 mg/kg.术后12,24,36,48,72 h,观察各组血清学及肝脏组织病理变化.结果与结论:①动脉化组与肝衰竭组均造模成功30只,术后72 h成活率分别为70%、53%,组间比较差异有显著性意义(P < 0.05);对照组术后72 h存活率为100%;②对照组不同时间点的血清门冬氨酸转氨酶、丙氨酸转氨酶、白细胞介素6、肿瘤坏死因子水平α及门静脉内毒素水平均低于其余两组(P < 0.05);动脉化组术后不同时间点的血清门冬氨酸转氨酶、丙氨酸转氨酶低于肝衰竭组(P < 0.05),术后24-72 h的总胆红素、白细胞介素6、肿瘤坏死因子水平α及门静脉内毒素水平均低于肝衰竭组(P < 0.05),36-72 h的白蛋白低于肝衰竭组(P < 0.05);③术后72 h,对照组肝脏结构完整;肝衰竭组正常肝小叶结构已破坏,大量炎细胞浸润;动脉化组病变清于肝衰竭组;④结果表明,门静脉动脉化可在一定程度上上改善肝脏功能,减缓肝衰竭的发展.%BACKGROUND: Partial portal vein arterialization (PPVA) can slow the progression of liver failure by increasing the blood supply. OBJECTIVE: To explore the effects of PPVA on the liver function and pathological changes in a rat model of liver failure.METHODS: Totally 130 Sprague-Dawley rats were randomized into three groups: PPVA group (n=50) underwent left nephrectomy, the PPVA model was established by sleeve suturing and cuff technology, and then D-galactosamine was intraperitoneally administered at the dose of 1 300 mg/kg to induce acute liver failure; liver failure group (n=50) underwent left nephrectomy, the portal vein was dissociated, ligated for 16 minutes and then mobilized, and D-galactosamine was intraperitoneally administered at the dose of 1 300 mg/kg to induce acute liver failure after abdominal closure; control group (n=30) received left nephrectomy, the portal vein was ligated for 16 minutes and then mobilized, and same volume of normal saline was intraperitoneally administered after abdominal closure. The serological and pathological changes of the liver tissue were observed at 12, 24, 36, 48 and 72 postoperative hours. RESULTS AND CONCLUSION: Animal models (n=30 per group) were made successfully, the survival rate was 70% and 53%, respectively, and there was a significant difference between two groups after modeling (P < 0.05). The survival rate in the control group was 100% at 72 postoperative hours. The serum levels of glutamic-oxalacetic transaminease, alanineaminotranferase, interleukin 6, tumor necrosis factor α, and endotoxin in the portal vein in the control group were significantly lower than those in the other two groups at different time points postoperatively (P < 0.05). In the PVA group, the serum levels of glutamic-oxalacetic transaminease and alanineaminotranferase at postoperative different time points postoperatively, the serum levels of total bilrubin, interleukin 6, tumor necrosis factor α, and endotoxin level in the portal vein at 24-72 postoperative hours, and albumin at 36-72 postoperative hours were significantly lower than those in the liver failure group (P < 0.05). At 72 postoperative hours, the liver structure was complete in the control group, hepatic lobules were damaged accompanied with abundant inflammatory cell infiltration in the liver failure group and the pathological lesions were improved in the PVA group. To conclude, PVA can improve liver function and slow the progression of liver failure to certain extents.

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