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Objective To explore the role of somatostatin in protecting small-for-size liver after hepatectomy in rats with cirrhosis.Methods Forty-eight rats with cirrhosis were randomly divided into somatostatin group (group S,n =24) and normal saline control group (group N,n =24).All rats from the two groups were measured with baseline portal vein pressure and blood flow volume.Additionally,at the endpoints of 15,30 and 60 min after ischemia/reperfusion with hepatic inflow occlusion,portal vein pressure and blood flow volume were detected from both groups.Liver function test was also measured at the endpoints of 1,3,5,24 h after ischemia/reperfusion for groups S and N.Results After 15-min ischemia/reperfusion,the portal vein pressure was higher in the rats of group S than that in group N [(19.4 ± 0.8) cmH2O vs.(22.5 ± 1.2) cmH2O (1 cmH2O =0.098 kPa)],there was significant difference (P ＜ 0.05).After 30 min ischemia/reperfusion,portal vein pressure results were (17.1 ± 0.8) cmH2O and (19.7 ± 0.8) cmH2O in group S and group N,respectively,P ＜ 0.05.At different endpoints,portal blood flow volume results were all higher in both groups than baseline figures.Furthermore,maximum portal blood flow volume was observed at the endpoint of 15 min ischemia/reperfusion in both groups,and lower in group S than group N [(10.1 ±0.4)ml/min vs.(11.9 ±0.5)ml/min,P＜0.05].Liver function test revealed AST,ALT,TBil exceed normal limits in rats of both groups,which elevated along prolonged ischemia/reperfusion.One week after hepatectomy,the survival of rats treated with somatostatin (group S,7/10) was superior to saline control group (group N,2/10),P ＜0.05.Future liver volume increased in rats from both groups,much significant increase was determined in group S [(5.5 ± 0.4) g vs.(6.6 ± 0.3) g,P ＜ 0.05].Conclusions Somatostatin might improve portal vein hypertension status in the early stage of small-for-size liver after hepatectomy,and decrease portal blood flow.Furthermore,it could alleviate small-for-size liver injury associated with portal vein hypertension and hyperperfusion,and benefit liver regeneration and improve postoperative survival in rats with cirrhosis.
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Objective To investigate the effects of different hepatic perfusion procedures for small-for-size liver transplantation in rats. Methods A total of 156 rats were randomly divided into two groups: portal vein perfusion group (groupⅠ, n=78) and abdominal aorta perfusion group (groupⅡ, n=78). After harvesting graft, the left lobe of the liver and the middle lobe were resected and the remaining approximately 30%volumes of the liver were transplanted in groupⅠand groupⅡ. The body weights of donor and acceptor, the weight of graft, the time of operating in donor, the cold ischemia time, anhepatic phase, the blocking time of inferior hepatic vena cava and the time of operating in receptor were recorded in two groups. The serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), pathological HE staining and 7-day survival rate in 6 h, 1 d, 3 d and 7 d after operation were compared between two groups. Results The serum levels of ALT and AST were decreased gradually in two groups, but the levels decreased slowly in groupⅠ. The serum levels of ALT and AST were significantly higher in groupⅠthan those of groupⅡ(P<0.05). HE staining showed greater damage of mi-crostructure of liver tissue at early stage in group Ⅰthan that in groupⅡ. The 7-day survival rate was lower in group Ⅰthan that of groupⅡ(χ2=4.050,P=0.044). Conclusion There is a higher survival rate and mild liver damage in small-for-size liver transplantation in rats using perfusion by abdominal aorta.
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Objective To establish small-for-size (SFS) graft injury models in miniature pigs with high standardization, reproducibility and similarity to clinical situation. Methods Ba-Ma miniature pigs were introduced in this study and orthotopic liver transplantations (OLTs) were performed in 12 pigs with 30% liver volume allogeneil grafts (small portion of right paramedian lobe, right lateral lobe and caudate lobe) without veno-venous bypass. The profiles of intra-operational hemodynamics and metabolism were investigated. Animals were observed for 7 days with daily serum biochemistry and coagulation function exam. The survival rate related to operation itself and the SFS grafts were respectively calculated as well as the graft regenerative ratio at post-operational day (POD) 7. Results Graft weight as a percentage of the recipient's native liver weight (GW/RLW) and the total body weight (GW/BW) were (28. 63±4. 42)% and (0. 73±0.06)%. The mean operation time, anhepatic phase, and the time of blockage of infra-hepatic IVC were (191. 7±14. 2) min, (28. 3±3. 6) min, and (45. 0±5. 8) min. The survival rate related to the operation itself and the SFS graft were 83. 33% (10/12) and 40% (4/10), and the graft regenerative ratio at POD7 was (278. 06±42. 95) %. Contrast to the remarkable increase of heart rate and serum potassium during anhepatic phase, the mean arterial pressure, central venous pressure, rectal temperature, PH value and buffer excess had a significant decrease (P<0.01) with a gradual recovery after reperfusioa Serum ALT, AST, PT, Cr, and TB were significantly increased with a peak level at POD1 for the former 4 and POD2 for TB, and then began to decrease and favorably recovered at POD7, but TB, PT, and AST levels were still high when compared to those of prereperfusion (P<0. 05). Conclusion This model of OLT performed with 30% liver volume graft without veno-venous bypass was an ideal large animal model for series studies related to SFS graft injury.
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Objective To introduce the mechanisms of graft injuries after small-for-size liver transplantation and protective measures.Methods Recently relevant literatures were reviewed and summarized.Results Portal hypertension after small-for-size liver transplantation induces mechanical injuries as well as hepatic sinusoidal microcirculation disturbance and cytokines release,which worsened the injuries.Decrease portal pressure by surgery or drug could improve grafts function.Conclusion Comprehending the mechanisms of graft injuries will contribute a lot for the living donor liver transplantation.