Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) provides hemodynamic rescue for patients encountering right or left ventricular (RV or LV) decompensation, particularly after surgery for congenital heart defects. ECMO, supported metabolically by parenteral nutrition, provides reductions in myocardial work and energy demand and therefore enhances functional recovery. The RV must often assume systemic ventricular pressures and function upon weaning from VA-ECMO. However the substrate utilization responses of the RV to VA-ECMO or stimulation are unknown. We determined RV and LV substrate utilization response to VA-ECMO in immature swine heart. Mixed breed male Yorkshire pigs (33-49 days old) underwent normal pressure volume loading (Ctrl, n=5) or unloaded by VA-ECMO (ECMO, n=10) for 8 hours. Five pigs with ECMO received intravenous thyroid hormone (T3) to alter substrate utilization. Carbon 13 (13C)-labeled substrates (lactate and medium-chain and long-chain fatty acids) were systemically infused as metabolic tracers. Analyses by nuclear magnetic resonance showed that both ventricles have similar trends of fractional 13C-labeled substrate contributions to the citric acid cycle under control conditions. VA-ECMO produced higher long-chain fatty acids and lower lactate contribution to the citric acid cycle via inhibition of pyruvate dehydrogenase, while T3 promoted lactate metabolism in both ventricles. However these metabolic shifts were smaller in RV, and RV fatty acid contributions showed minimal response to perturbations. Furthermore, VA-ECMO and T3 also achieved high [phosphocreatine]/[ATP] and low [NADH]/[NAD+] in LV but not in RV. These data suggest that the RV shows decreased ability to modify substrate utilization and achieve improvements in energy supply/demand during VA-ECMO.
- cardiac metabolism
- extracorporeal circulation
- thyroid hormone
- Copyright © 2017, American Journal of Physiology-Heart and Circulatory Physiology