| Objective: Chinese liver disease incidence was one of the most highest countries in the world. It suffering our people seriouslay, that hepatitis, hepatic cirrhosis and hepatoma damage liver uncovertable and lead to final liver disease stage. With the development of surgical techniques organ preservation amboperation therapy and transplantation immunology molecular biology, liver transplantation became the ultimatet way to cure final liver disease. But the receptors usually had many complications during perioperative period , pulmonary dysfunction and multiple system organ failure were the most dangerous complications after operation. In this experiment, we imtate the anhepatic of clinical OLT ,try to find the effect of Xuebijing and its character mechanism of pulmonary I/R injury during anhepatic phase. So we could give effective treatment to…the receptor of pulmonary complications after OLT.Methods: 110 healthy male Wistar rats, weighted 250-300g, were used. 15 rats were taken randomly as normal rats, recoverable prehepatic portal hypertensive models were generated on the other rats through the first operation which partly narrow portal vein and let the"mark ring"in. 3 weeks later, all the models generated successfully. 5 were used to justify portal hypertension models, another 5 rats were from normal rats .Portal pressure portovenography and the area of esophageal submucosal veins were measured in the above two groups. Last 10 normal rats as a sham operation group (SOG),and 90 model rats were divided into 3 groups, inject NS, Xuebijing, ulinastatin through vena caudalis, three days later each group was performed the second operation: blocking hepatic hilum inferior vena , unclamping 60min later. Arterial PaO2 and venous AST ALT level were measured. Myeloperoxidase(MPO) activity in lung tissue, wet-to-dry weight rations of lung were measured. Morphology changes of liver and lung were microscope. All experimental data were analyzed by statistic software of SPSS 12.0.Results:Three weeks later after the first operation ,all the portal hypertensive model rats were generated successfully. Ascites and varices of vscera could be seen in the PHM rats, but the color and texture of liver were normal. The free portal pressure of PHM rats were 15.6±3.1mmHg ,was obviously higher than that of normal rats(7.7±1.7mmHg), and the difference was significant (P<0.05).The portovenography of PHM rats showed that development of liver was slow , and a stenosis could be seen at the portal vein trunk proximal to the bifurcation, the vessels of portal system twisted and azygos vein could be seen , the superior and inferior vena cava through the portosystemic shunt developed, the stenosis of portal vena disappeared after removed the"mark ring". There were no shunts between portal and vena cava system in normal rats . the area of esophageal submucosal veins of normal rats and PHM rats were 5.620±1.301μm2 and33.582±6.425μm2 (P<0.05).In I/R group AST ALT MPO of lung tissue wet -to-dry weight ratios were higher than the other groups;PaO2 of Xuebijing and ulinastatin group are higher than I/R group but lower than SO group; By optical microscopy , the structure of lung is disorder the septum of alveolus became wider, and part of the pulmonary alveolus was atrophic intra-alveolus and interstitial edema with inflammatory cells infiltrating was obvious. The lightest pathological changes were in Xuebijing and ulinastatin group. Xuebijing group had no obviously differences to ulinastatin group.Conclusion: The method in our experiment can successfully generate the model of recoverable prehepatic portal hypertention in the rats, which was simple duplicated reliable and initiative.It could be applied for the basic study on OLT. Xuebijing and ulinastatin could decrease the MPO activity of lung tissue protect lung blood capillary. During anhepatic phase and the ischemia-reperfusion injury oxidation or antioxidation is the main factor especially, which caused lung tissue injury. Xuebijing can protect lung tissue by inhibit heterophil granulocyte activity and antioxidation.
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