Document Detail


Extracorporeal membrane oxygenation promotes long chain fatty acid oxidation in the immature swine heart in vivo.
MedLine Citation:
PMID:  23727393     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Extracorporeal membrane oxygenation (ECMO) supports infants and children with severe cardiopulmonary compromise. Nutritional support for these children includes provision of medium- and long-chain fatty acids (FAs). However, ECMO induces a stress response, which could limit the capacity for FA oxidation. Metabolic impairment could induce new or exacerbate existing myocardial dysfunction. Using a clinically relevant piglet model, we tested the hypothesis that ECMO maintains the myocardial capacity for FA oxidation and preserves myocardial energy state. Provision of 13-Carbon labeled medium-chain FA (octanoate), long-chain free FAs (LCFAs), and lactate into systemic circulation showed that ECMO promoted relative increases in myocardial LCFA oxidation while inhibiting lactate oxidation. Loading of these labeled substrates at high dose into the left coronary artery demonstrated metabolic flexibility as the heart preferentially oxidized octanoate. ECMO preserved this octanoate metabolic response, but also promoted LCFA oxidation and inhibited lactate utilization. Rapid upregulation of pyruvate dehydrogenase kinase-4 (PDK4) protein appeared to participate in this metabolic shift during ECMO. ECMO also increased relative flux from lactate to alanine further supporting the role for pyruvate dehydrogenase inhibition by PDK4. High dose substrate loading during ECMO also elevated the myocardial energy state indexed by phosphocreatine to ATP ratio. ECMO promotes LCFA oxidation in immature hearts, while maintaining myocardial energy state. These data support the appropriateness of FA provision during ECMO support for the immature heart.
Authors:
Masaki Kajimoto; Colleen M O'Kelly Priddy; Dolena R Ledee; Chun Xu; Nancy Isern; Aaron K Olson; Michael A Portman
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural     Date:  2013-05-30
Journal Detail:
Title:  Journal of molecular and cellular cardiology     Volume:  62     ISSN:  1095-8584     ISO Abbreviation:  J. Mol. Cell. Cardiol.     Publication Date:  2013 Sep 
Date Detail:
Created Date:  2013-08-05     Completed Date:  2013-12-11     Revised Date:  2014-09-02    
Medline Journal Info:
Nlm Unique ID:  0262322     Medline TA:  J Mol Cell Cardiol     Country:  England    
Other Details:
Languages:  eng     Pagination:  144-52     Citation Subset:  IM    
Copyright Information:
Copyright © 2013 Elsevier Ltd. All rights reserved.
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MeSH Terms
Descriptor/Qualifier:
Animals
Extracorporeal Membrane Oxygenation*
Fatty Acids / metabolism*
Heart
Hemodynamics
Immunoblotting
Magnetic Resonance Spectroscopy
Male
Myocardium / metabolism*
Oxidation-Reduction
Swine
Grant Support
ID/Acronym/Agency:
R01 HL060666/HL/NHLBI NIH HHS; R01HL60666/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Fatty Acids
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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