Examination of protective effect of ischemic postconditioning after small bowel autotransplantation.

Ischemia/reperfusion (I/R) injury is a serious condition that results from some surgical procedures, including intestinal transplantation. Ischemic postconditioning is defined as brief periods of reperfusion alternating with reocclusion applied during the early minutes after reperfusion. The objective of this study was to investigate the effect of ischemic postconditioning before small bowel autotransplantation. Total orthotopic intestinal autotransplantation was performed in 30 white domestic pigs. Grafts were stored in cold University of Wisconsin solution for 1, 3, or 6 hours. Duration of reperfusion was 3 hours in all grafts. Before reperfusion, the intestine was postconditioned via 3 cycles of ischemia for 30 seconds and reperfusion for 30 seconds (ischemic postconditioning protocol). Tissue from the small intestine was obtained after laparotomy (control group) and at the end of reperfusion periods. To monitor oxidative stress, tissue concentrations of malondialdehyde and reduced glutathione, and activity of superoxide dismutase were determined at spectrophotometry. Tissue damage on sections stained with hematoxylin- eosin was evaluated using a quantitative method (Scion Image software; Scion Corp, Frederick, Maryland). Our results demonstrated that ischemic postconditioning significantly decreased the reperfusion-ended lipid peroxidation value (mean +/- SEM, 142.0 +/- 7.1 micromol/g vs 125.0 +/- 2.1 micromol/g; P < .05). Moreover, the capacity and activity of endogenous antioxidant protective systems (glutathione 789+/-8.0 micromol/g vs 934 +/- 5.7 micromol/g, and superoxide dismutase 110 +/- 9 IU/g vs 126 +/- 4 IU/g; P < .05) remained higher in the ischemic postconditioning groups compared with tissues without ischemic postconditioning. At quantitative analysis, tissue injury was increased by the duration of cold preservation. The greatest injury was observed in the mucosal and submucosal layers and in the depth of crypts after 6 hours of preservation. Ischemic postconditioning significantly decreased intestinal wall injury in each group (P < .05). It was concluded that ischemic postconditioning before reperfusion mitigated oxidative stress and histologic damage during small bowel autotransplantation.

[Treatment of obstruction of extrahepatic biliary pathways by antireflux, bilio-cholecystic (cystico) enteroanastomosis methods].

The main target of our investigations was the development of antireflux, bilio-cholecysto (cystico) enteral anastomosis method for the surgical treatment of extrahepatic biliary duct obstruction. We were using the cholecystic duct spiral valve (Lutkens valve, Haister valve) as the antireflux structure. In this case the bile drains into the biliary cyst not through the cholecystic duct but through the extrahepatic biliary duct - the bilio-cholecystic anastomosis. Such an interposition of cholecystic and spiral valves promotes inhibition of chemical reflux between extrahepatic ducts and gastrointestinal tract, from digestive tract into the cholecystic and intrahepatic biliary tracts. Method developed and tested by us involves creation of blio-cholecystic (cystico) entero anastomosis, namely creation of biliary duct-cholecystic (cystico)-duodenoanastomosis. 3 successful experimental operations have been performed using the above presented approach. Sutures were taken of on the seventh day, animals were housed under investigations for 10-14 days, faecal masses had normal appearance.

Toxic acute liver failure treatment by isolated hepatocytes allotransplantation in experimental.

Acute liver failure treatment nowadays is a common problem in modern hepatology, despite of well studied pathogenesis and treatment modalities, lethality of the disease is still high, and in 21 century in the world's best clinics it accounts to 70-80%. For uptake of isolated hepatocytes we uses the fermental-mechanical method modified by Korukhov (1983) for the treatment of acute liver failure by hepatocyte allotransplantation and to stimulate liver reparative regeneration processes, which gives a chance to liver for the function restoration by replacement of injured hepatocytes with transplanted liver cells. We provide experiments on 45 white laboratory Vistar line rats (150-200gr) which were kept on standard environment, animals were divided into three equal groups: I group (n=20) was served as a control group, in which we provide acute liver failure modelling, by toxic agent (carbontetrachloride CCL4 ) treatment by naso-gastric tube, After acute liver failure modelling, in the II group (n=20) of animals we were conducting liver cell transplantation, III group (n=5) animals were served as donors for isolated hepatocyte uptake. Cell ultrastructure element proliferation clearly seen by morphological evaluation and animals which have acute liver failure had a chance for survival and it may be concluded that our proposed method can be the curative treatment method of acute liver failure in experiment.