EFFECTS OF GLUTAMATE AND ASPARTATE ON MYOCARDIAL SUBSTRATE OXIDATION DURING POTASSIUM ARREST

Objectives: A recent report (J Clin Invest 1993;92:831-9) found no eff ect of glutamate plus aspartate on metabolic pathways in the heart, bu t the experimental conditions did not model clinical cardioplegia, The purpose of this study was to determine the effects of glutamate and a spartate on metabolic pathways feeding the citric acid cycle during ca rdioplegic 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 substr ates were enriched with C-13, which allowed a complete analysis of sub strate oxidation by C-13-nuclear magnetic resonance spectroscopy in on e experiment, Three groups of hearts were studied: arrest with potassi um cardioplegic solution, arrest with cardioplegic solution supplement ed with glutamate and aspartate (both in concentrations of 13 mmol/L), and a control group without cardioplegic arrest, Results: In potassiu m-arrested hearts, the contributions of fatty acids and lactate to ace tyl coenzyme A were reduced, and acetoacetate was the preferred substr ate for oxidation in the citric acid cycle, The addition of aspartate and glutamate in the presence of cardioplegic arrest did not further a lter patterns of substrate utilization substantially, although acetoac etate use was somewhat lower than,vith simple cardioplegic arrest, Whe n [U-C-13]glutamate (13 mmol/L) and [U-C-13]aspartate (13 mmol/L) were supplied as the only compounds labeled with C-13, little enrichment i n citric acid cycle intermediates could be detected. Conclusions: Glut amate and aspartate when added to potassium cardioplegic solutions hav e relatively minor effects on citric acid cycle metabolism.