Protective Effect Of Ischemic Preconditioning On The Hepatic Ischemia-Reperfusion And Lung Injury In Rats

Protection from ischemia-reperftisiofl is a basic theme faced with clinical situation, plays an impotant role in infection, trauma, shock, pulmonary and cardic dysfunction, liver transplantation and so on. Hepatic ischemia reperfusion not only causes liver injury , but also promotes the translocation of bacteria and endotoxin from the gut into portal vein, activate reticuloendothelial system, release mediators and cytokines, which cause multiple organ failure, among them, the acute pulmonary injury is common and severe. Study of protective effect shows mechanisms and new theory for hepatic ischemia reperfusion injury. A short period of ischemia and reperfusion, called ischemic preconditioning, protects various tissues against subsequent sustained ischemic insults. Ischemic preconditiofliflg have been ubiquitous. ActalLy, ischemic preconditioning confers a state of adaption for various tissues and organs and changes mediators and cytokines in tissues and organs, the mechanisms by which ischemic preconditioning promotes adaptability of tissues and organs to sustained ischemic insults. The purpose of this study is to investigate the protective effect of ischemic preconditiofling on the hepatic ischemic-reperfusiofl and lung injury in rats, and relationsip between ischemic preconditioning and tumor necrosis factor- a hepatocyte apoptosis, neutrophils, so as to provide the experimental data and ?-? academic foundations for hepatobiliary deseases. The main research methods and results in the study as follows: 1. Partial hepatic ischemia model was utilized to produce severe ischemic liver damage without intestinal congestion. Results showed that partial hepatic ischemic model prevented mesenteric veinous congestion and intestinal injury by permitting portal decompression through the right lobe. All structures in the portal triad (hepatic artery, portal vein, and bile duct) to the left and median liver lobes were occluded in bloc for the denifite time under study, so as to decrease portal triad damage brought with the skeleton of portal triad. 2. A nontraumatic vascular clamp was applied to interupt liver pedicle to the left and median liver lobes for 5-1 5mm ischemia-reperfusion., then the liver pedicle was occluded for 60mm for the second time. 3. ATP, ADP, AMP, adeno sine aspartate and alanine aminotrasferase were examined to detect the best method and time for ischemic preconditioning of liver. Results showed that in conparison with control group, ischemic preconditioning ameliorated hepatic ischemic-reperfusion injury in rats. A single ischemia of 10mm and reperfusion period of 10mm before 60mm warm ischemia maintained ATP and adenosine in hepatic tissure, decreased the concentrations of aminotransferase in blood, suggested that a single ischemia of 1 0mm and reperfusion period of 1 0mm produced the best protective effect on liver injury in the rats. 4. Terminal deoxynucleotidy I transferase- mediated dUTP nick end labeling deoxynucleotidyl transferase(TU7NEL), electron microscope, and DNA fragmentation gel electrophoresis Were utilized to monitor hepatocytes in hepatic ischemic preconditioning and ischemia-reperfusion. In this study , we have demastrated that apoptosis of hepatocytes occurs after reperfusion following warm ischemia. EM and DNA fragmentation gel electrophoresis...