title: Myocardial substrate oxidation during warm continuous blood cardioplegia.
abstract: BACKGROUND
  Although long-chain fatty acids are a major energy substrate utilized by the myocardium, changes in the substrate balance toward a predominating fatty acid utilization could jeopardize the myocardium during cardiac operative procedures.
  
  
  METHODS
  In the present study myocardial substrate utilization was examined during warm continuous blood cardioplegia (4 hours, 37 degrees C), using pigs undergoing cardiopulmonary bypass. Hearts were perfused antegradely in a closed extracorporeal circuit in which cardioplegic donor blood (hematocrit, 22%) containing 14C-glucose and 3H-oleate was delivered to the heart. Arterial and coronary sinus blood samples were taken at intervals for determination of plasma concentrations of energy substrates, as well as glucose and oleate oxidation rates (14CO2 and 3HOH production).
  
  
  RESULTS
  The concentration of fatty acids in the cardioplegic perfusate did not change significantly during the cardiac arrest period. The mean concentration of glucose showed a 30% decline (not significant), whereas the lactate concentration increased from a starting value of 3.12 +/- 0.27 to 6.31 +/- 0.72 mmol/L at the end (mean +/- standard error of the mean; n = 8; p < 0.05). Only fatty acid levels showed a significant (positive) arterial-coronary sinus difference. Myocardial oxidation of oleate varied between 302 +/- 71 and 650 +/- 66 nmol.min-1.heart-1, whereas the range of variation for glucose oxidation was 144 +/- 64 to 355 +/- 107 nmol.min-1.heart-1. However, the changes in fatty acid levels and glucose oxidation rates during the cardiac arrest period were not statistically significant. We calculated that overall glucose oxidation accounted for less than 5% of the total aerobic energy production.
  
  
  CONCLUSIONS
  The present results demonstrate overreliance on fatty acids as a source of energy during warm continuous blood cardioplegia, consistent with a condition of myocardial insulin resistance.
authors.affiliation: Department of Medical Physiology, Faculty of Medicine, University of Tromsø, Norway.
authors.forename: T S
authors.initials: TS
authors.lastname: Larsen
authors.forename: O
authors.initials: O
authors.lastname: Irtun
authors.forename: T K
authors.initials: TK
authors.lastname: Steigen
authors.forename: T V
authors.initials: TV
authors.lastname: Andreasen
authors.forename: D
authors.initials: D
authors.lastname: Sørlie
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D000818:Animals; D001769:Blood; D004734:Energy Metabolism; D005230:Fatty Acids, Nonesterified / Q000378:metabolism; D005260:Female; D005947:Glucose / Q000378:metabolism*; D006324:Heart Arrest, Induced / Q000379:methods; D006454:Hemoglobins / Q000032:analysis; D007773:Lactates / Q000378:metabolism; D019344:Lactic Acid; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D019301:Oleic Acid; D009829:Oleic Acids / Q000378:metabolism*; D010084:Oxidation-Reduction; D010101:Oxygen Consumption; D013552:Swine; D013696:Temperature
chemical_list: D005230:Fatty Acids, Nonesterified; D006454:Hemoglobins; D007773:Lactates; D009829:Oleic Acids; D019301:Oleic Acid; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D005947:Glucose