Abstract 12393: Effects of Continuous Triiodothyronine Infusion on Citric Acid Cycle in the Normal Immature Swine Heart under Extracorporeal Membrane Oxygenation in vivo
Background: Extracorporeal membrane oxygenation (ECMO) is frequently used in infants with postoperative cardiopulmonary failure. ECMO also suppresses circulating triiodothyronine (T3) levels and modifies myocardial metabolism. We assessed the hypothesis that T3 supplementation reverses ECMO induced metabolic abnormalities in the immature heart.
Methods and Result: Twenty-two male Yorkshire pigs (age 25-38 days) with ECMO were received [2-13C]lactate, [2,4,6,8-13C]octanoate (medium-chain fatty acid) and [U-13C]long-chain fatty acids as metabolic tracers either systemically (totally physiological intracoronary concentration) or directly into the coronary artery (high fatty acid concentration) for last 60 minutes of each protocol. Nuclear magnetic resonance (NMR) analysis of left ventricular tissue determined the fractional contribution (Fc) of these substrates to the citric acid cycle (CAC). Intravenous T3 supplement (a bolus at 0.6 μg/kg and then continuous infusion at 0.2 μg/kg/hour) was given half of the pigs during ECMO. T3 increased lactate-Fc and decreased octanoate-Fc relatively. However high fatty acid study showed that only lactate-Fc was decreased by T3, whereas octanoate-Fc was not altered by T3, providing more than 60% of the CAC oxidation via acetyl-CoA. Both T3 and high fatty acids increased myocardial energy status indexed by [Phosphocreatine]/[ATP].
Conclusions: T3 supplemention promoted lactate metabolism to the CAC during ECMO. This effect supports prior studies showing that T3 releases inhibition of pyruvate dehydrogenase. Manipulation of substrate utilization by T3 may be used therapeutically during ECMO to improve resting energy state and facilitate weaning.
- © 2013 by American Heart Association, Inc.