Portal vein arterialization for acute hepatic failure in rats / 中国组织工程研究

ABSTRACT

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.