title: Post-conditioning preserves glycolytic ATP during early reperfusion: a survival mechanism for the reperfused heart.
abstract: BACKGROUND
  Glycolytic activity during the transition period from anaerobic to aerobic metabolism has been demonstrated to be critical for heart recovery in isolated reperfused hearts. The purpose of this work was to investigate the relevance of the glycolytic pathway in preserving the cardiac function of post-conditioned hearts.
  
  
  METHODS
  The activation of the glycolytic pathway in post-conditioned hearts was evaluated by measuring GLUT-4 insertion, glucose consumption and lactate production. Iodoacetic acid and 2-deoxy-D-glucose were administrated to the working hearts to evaluate the effect of glycolytic inhibition in the post-conditioning protective effect.
  
  
  RESULTS
  Post-conditioning maneuvers applied to isolated rat hearts, after prolonged ischemia and before reperfusion, promoted recovery of cardiac mechanical function with sustained increase of GLUT-4 translocation and activation of the glycolytic pathway during ischemia and early reperfusion. Iodoacetate inhibited the protective effect of post-conditioning, without affecting the mitochondrial oxidative capacity. Glycolysis contribution to maintain mechanical function at early reperfusion was observed in post-conditioned hearts perfused with 2-deoxy-D-glucose and in hearts in which iodoacetate was administered only during reperfusion.
  
  
  CONCLUSIONS
  It is concluded that in the post-conditioned heart, a functional compartmentation of anaerobic energy metabolism, at early reperfusion, plays a significant role in cardiac protection against reperfusion damage.
authors.affiliation: Departamento de Bioquimica, Instituto Nacional de Cardiologia, México DF, Mexico.
authors.forename: Francisco
authors.initials: F
authors.lastname: Correa
authors.forename: Noemí
authors.initials: N
authors.lastname: García
authors.forename: Juan
authors.initials: J
authors.lastname: Gallardo-Pérez
authors.forename: Liliana
authors.initials: L
authors.lastname: Carreno-Fuentes
authors.forename: Sara
authors.initials: S
authors.lastname: Rodríguez-Enríquez
authors.forename: Alvaro
authors.initials: A
authors.lastname: Marín-Hernández
authors.forename: Cecilia
authors.initials: C
authors.lastname: Zazueta
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D003600:Cytosol / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D051275:Glucose Transporter Type 4 / Q000378:metabolism; D006019:Glycolysis; D006321:Heart / Q000502:physiology* / Q000503:physiopathology; D006593:Hexokinase / Q000378:metabolism; D066298:In Vitro Techniques; D019344:Lactic Acid / Q000096:biosynthesis; D008297:Male; D015425:Myocardial Reperfusion; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology; D009206:Myocardium / Q000201:enzymology; D010725:Phosphocreatine / Q000378:metabolism; D021381:Protein Transport; D051381:Rats; D017208:Rats, Wistar; D012508:Sarcolemma / Q000378:metabolism
chemical_list: D051275:Glucose Transporter Type 4; D010725:Phosphocreatine; D019344:Lactic Acid; D000255:Adenosine Triphosphate; D006593:Hexokinase; D005947:Glucose