Repair And Protective Effect And Mechanisms Of Extracorporeal Membrane Oxygenation On Donation After Cardiac Death Liver Graft

Objective: To prove the protective effects of extracorporeal membrane oxygenation(ECMO) on donation after cardiac death(DCD) liver graft and explore the mechanisms.Methods:1. Eight pigs were used. Cardiac arrest was induced by administration of 1g KCL,followed by 30 min of cardiopulmonary resuscitation. Cannulas were inserted into inferior vena cava and abdominal aorta,then connected to the ECMO equipment. ECMO perfomed for 4h. Circulation flow rate of hepatic artery and bile production were monitored and recorded. Lactate dehydrogenase(LDH) and ?-glutamyl transferase(?-GT) in bile were detected.Transaminase, Tumor necrosis factor-?(TNF-?),Interleukin-1?(IL-1?),Hyaluronic acid(HA),Endothelin-1(ET-1) and Nitric oxide(NO) in serum were detected at the time of baseline,death announcement and ECMO 4h. Pathological changes of liver tissue and bile duct tissuewere observed by HE stain under optical microscope.2. Twelve pigs were randomized to ECMO group and control group, six pigs per group. Cardiac arrest was induced by administration of 1g KCL, followed by 30 min of cardiopulmonary resuscitation. Cannulas were inserted into inferior vena cava and abdominal aorta, then connected to ECMO equipment in ECMO group for 4h. The livers were stored in cold UW for 4h in control group after cardiac death. ATP, e NOS, SOD, GSH, MDA, adenosine and HSP70 were detected in liver tissue at the time of baseline, death announcement, ECMO4 h and cold preservation 4h. Pathological change was observed by electron microscopy.Results:1. Blood flow of hepatic artery after cardiac arrest decrease rapidly, but returned to the baseline level soon after ECMO recycle started and remained stable during ECMO recycle. There was no bile production after cardiac death, but it returned to 80% of baseline after 4h of ECMO recycle. There was no statistically significant difference between ECMO 4h and baseline on the level of ?-GT, LDH in bile and IL-1?, TNF-?, HA in serum(P> 0.05). There was statistically significant difference between ECMO 4h and baseline on the level of ET-1 and NO(P<0.05). Pathological changes of liver and bile duct afte 4h of ECMO were significantly better than those after cardiac death.2. Tissue ATP decreased to less than 40% of baseline after 30 minutes of warm ischemia and returned to baseline after 4h, while ATP of control group continued a further decline. Compared with control group, SOD?GSH and HSP70 increased significantly in ECMO group(P<0.05), while MDAdecreased significantly(P<0.05). Compared with baseline, e NOS increased significantly in ECMO group(P<0.05), whiledecreased significantly in control group(P<0.05)?There was statistically significant difference on the level of e NOS between ECMO group and control group(P < 0.05). Pathological changes of liver tissue observed by electron microscopy in ECMO group were significantly better than those in control group.Conclusion: 1. There is significant protective effect of extracorporeal membrane oxygenation on liver and bile duct after cardiac death.2. ECMO can supply oxygen and nutrients to liver after warm ischemian and increase energy reserve. ECMO has ischemiapreconditioning effect by upregulating adenosine and NO. By increasing GSH, SOD and HSP70 and other protective proteins, ECMO alleviates oxidative stress and liver damage.