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J Thorac Cardiovasc Surg 1996;112:1651-1660
© 1996 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

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

Supported by Grant-in-Aid 94013300 from the American Heart Association, the Southwestern Biomedical magnetic Resonance Facility Grant (NIH P41 RR-02584), and the Department of Veterans Affairs Clinical Investigator Program.

Presented in part at the Eightieth Clinical Congress of the American College of Surgeons, October 1994.

Received for publication April 22, 1996 Revisions requested June 7, 1996; revisions received June 24, 1996 Accepted for publication June 24, 1996. Address for Reprints: Michael E. Jessen, MD, Division of Thoracic and Cardiovascular Surgery, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd., Dallas, TX 75235-8879.

Abstract

Objectives: 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. (J THORACCARDIOVASCSURG1996;112:1651-60)

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