Repair mechanism of extracorporeal membrane oxygenation on liver after cardiac death / 中华器官移植杂志

ABSTRACT

Objective To study the repair mechanism of extracorporeal membrane oxygenation on liver after cardiac death.Methods Twelve pigs were equally randomized to ECMO group and control group.Cardiac arrest was induced by administration of 1 g KCL intravenously,followed by 30 min cardiopulmonary resuscitation according to the standard guideline Cannulas were placed through inferior vena cava and abdominal aorta,then connected to ECMO extracorporeal circulation pipes in ECMO group for 4 h.The livers were stored in cold UW for 4 h in control group.ATP,superoxide dismutase (SOD),glutathionein (GSH),malondialdehyde (MDA),heat shock protein 70 (HSP70) and intercellular cell adhesion molecule-1 (ICAM-1) were detected in liver tissue.Pathological change was observed by optical microscope and electron microscopy.Results Tissue ATP decreased to less than 40％ of baseline after 30 min of warm ischemia,then restored to 70％ after 2 h of ECMO and returned to baseline after 4 h,while ATP of control group continued a further decline As compared with control group,SOD,GSH and HSP70 increased significantly in ECMO group (P＜0.05),while MDA and ICAM-1 decreased significantly (P＜0.05).Pathological changes of liver tissue observed by optical microscope and electron microscopy in ECMO group were significantly were significantly alleviated as compared with those in control group.Conclusion ECMO can supply oxygen and nutrients to liver after warm ischemia and increase energy reserve.By upregulating GSH,SOD and HSP-70 and other protective proteins,ECMO alleviates oxidative stress and liver damage ECMO also improves microcirculation and reduces neutrophil infiltration by protecting sinusoidal endothelial cells.