TITLE:
The Apoptotic and Inflammatory Response of Brain Striatal Tissue to Extracorporeal Membrane Oxygenation (ECMO) Following the Model of Cardiac Arrest in Young Piglets
AUTHORS:
Peter Pastuszko, Gregory Schears, Joanna Kubin, David Franklin Wilson, Anna Pastuszko
KEYWORDS:
Brain, ECMO, Apoptosis, Inflammation
JOURNAL NAME:
World Journal of Cardiovascular Diseases,
Vol.11 No.11,
November
16,
2021
ABSTRACT: We investigated the effects of ECMO on pro-apoptotic and pro-inflammatory signaling in the striatum of piglets following cardiac arrest. 3-week-old pigletswereanesthetized, 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 pigletswereeuthanized 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 partiallyprotect 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.