The Apoptotic and Inflammatory Response of Brain Striatal Tissue to Extracorporeal Membrane Oxygenation (ECMO) Following the Model of Cardiac Arrest in Young Piglets

We investigated the effects of ECMO on pro-apoptotic and pro-inflammatory signaling in the striatum of piglets following cardiac arrest. 3-week-old piglets were anesthetized, paralyzed and ventilated. Oxygen in the ventilated gas was decreased from 21% to 7% - 10% over 30 min, then ventilation stopped until cardiac arrest. Three minutes after arrest, resuscitation began in two groups, without ECMO (CA) and with ECMO (ECMO). In a control group (C), the animals were sham operated. After 6 hours of recovery, the piglets were euthanized and stratum harvested. Measurement of apoptotic and inflammatory proteins was performed by RayBiotech, Inc. The results are means (6) ± SEM. There were no differences between CA and ECMO groups for anti-apoptotic proteins. ECMO significantly decreased pro-apoptotic proteins (Bax, cytoC, IGFBP-6, TNF-beta and TRAIR 1 and 3) as compared to CA group. Bcl-2 to Bax ratio increased in ECMO group suggesting that ECMO can least partially protect striatum from apoptotic injury. With respect to inflammation, ECMO significantly decreased both anti-inflammatory (ANG-1, FGF-21, IFN-alpha and beta, IGF-2, IL-10, IL-13, IL-1ra, IL-22, IL-4, IL-6, NCAM-1, SCF, TGF-alpha, TIMP-1and 2, VECF) and pro-inflammatory proteins (IL-12p40, IL-21, IL-15, IL-1 alpha and beta, IL-8, MIP-1 beta, OPG, PIGF-2, RANTES and TGF beta) in striatum of piglets. Conclusions: In a piglet model of cardiac arrest, ECMO significantly reduced levels of pro-apoptotic proteins without changing the levels of anti-apoptotic proteins. ECMO also significantly decreased the levels of both pro- and anti-inflammatory proteins. This decrease in the levels of both pro- and anti-inflammatory proteins may lead to disturbed neuronal metabolism and amplify inflammatory cell death.