title: Effects of glutamate and aspartate on myocardial substrate oxidation during potassium arrest.
abstract: OBJECTIVE
  A recent report (J Clin Invest 1993;92:831-9) found no effect of glutamate plus aspartate on metabolic pathways in the heart, but the experimental conditions did not model clinical cardioplegia. The purpose of this study was to determine the effects of glutamate and aspartate on metabolic pathways feeding the citric acid cycle during cardioplegic arrest in the presence of physiologic substrates.
  
  
  METHODS
  Isolated rat hearts were supplied with fatty acids, lactate, pyruvate, glucose, and acetoacetate in physiologic concentrations. These substrates were enriched with 13C, which allowed a complete analysis of substrate oxidation by 13C-nuclear magnetic resonance spectroscopy in one experiment. Three groups of hearts were studied: arrest with potassium cardioplegic solution, arrest with cardioplegic solution supplemented with glutamate and aspartate (both in concentrations of 13 mmol/L), and a control group without cardioplegic arrest.
  
  
  RESULTS
  In potassium-arrested hearts, the contributions of fatty acids and lactate to acetyl coenzyme A were reduced, and acetoacetate was the preferred substrate for oxidation in the citric acid cycle. The addition of aspartate and glutamate in the presence of cardioplegic arrest did not further alter patterns of substrate utilization substantially, although acetoacetate use was somewhat lower than with simple cardioplegic arrest. When [U-13C]glutamate (13 mmol/L) and [U-13C]aspartate (13 mmol/L) were supplied as the only compounds labeled with 13C, little enrichment in citric acid cycle intermediates could be detected.
  
  
  CONCLUSIONS
  Glutamate and aspartate when added to potassium cardioplegic solutions have relatively minor effects on citric acid cycle metabolism.
authors.affiliation: Department of Surgery, University of Texas Southwestern Medical Center at Dallas 75235-8879, USA.
authors.forename: M K
authors.initials: MK
authors.lastname: Reed
authors.forename: C
authors.initials: C
authors.lastname: Barak
authors.forename: C R
authors.initials: CR
authors.lastname: Malloy
authors.forename: S P
authors.initials: SP
authors.lastname: Maniscalco
authors.forename: M E
authors.initials: ME
authors.lastname: Jessen
mesh_terms: D000090:Acetoacetates / Q000378:metabolism; D000818:Animals; D001224:Aspartic Acid / Q000494:pharmacology*; D002250:Carbon Radioisotopes; D002952:Citric Acid Cycle / Q000187:drug effects*; D005227:Fatty Acids / Q000378:metabolism; D005947:Glucose / Q000378:metabolism; D018698:Glutamic Acid / Q000494:pharmacology*; D006321:Heart / Q000187:drug effects*; D006324:Heart Arrest, Induced / Q000379:methods*; D066298:In Vitro Techniques; D019344:Lactic Acid / Q000378:metabolism; D009682:Magnetic Resonance Spectroscopy; D008297:Male; D009206:Myocardium / Q000378:metabolism*; D010084:Oxidation-Reduction / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects; D011188:Potassium; D019289:Pyruvic Acid / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000090:Acetoacetates; D002250:Carbon Radioisotopes; D005227:Fatty Acids; D001224:Aspartic Acid; D019344:Lactic Acid; D018698:Glutamic Acid; C016635:acetoacetic acid; D019289:Pyruvic Acid; D005947:Glucose; D011188:Potassium