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J Thorac Cardiovasc Surg 2000;119:1030-1038
© 2000 The American Association for Thoracic Surgery

Cardiopulmonary Support And Physiology

Captopril-induced glutamate release at the start of reperfusion after cold cardioplegic storage of pig hearts

From the Department of Cardiology and Institute of Experimental Clinical Research, Skejby Hospital, Aarhus University Hospitals, University of Aarhus, Denmark.

Supported by the Danish Health Research Council, grant No. 9600822 (Aarhus University, Novo Nordisk Centre for Research in Growth and Regeneration).

Address for reprints: Flemming Randsbæk, MD, Department of Cardiology, Skejby Hospital, Aarhus University Hospitals, Brendstrupgaardvej, 8200 Aarhus N, Denmark.

Objective: We sought to evaluate the effects of captopril on glucose-related metabolism during hypothermic cardioplegic storage and subsequent reperfusion.
Methods: We compared hearts from control pigs with hearts from pigs treated with increasing oral doses of captopril for 3 weeks (12.5-150 mg daily), an intravenous bolus (25 mg) before operation, and captopril-containing cardioplegic solution (1 mg/L). The hearts were excised after infusion of cold crystalloid cardioplegic solution and stored in saline solution (4°C-6°C). In one series we studied myocardial blood flow and arteriovenous differences in oxygen, glucose, lactate, glutamate, and alanine during 60 minutes of postcardioplegic blood reperfusion. In this series captopril-treated hearts were reperfused with captopril-containing blood (1 mg/L). In another series we obtained biopsy specimens from the left ventricle throughout 30 hours of hypothermic cardioplegic storage and monitored tissue content of energy-rich phosphates, glycogen, glutamate, and alanine.
Results: Captopril increased glutamate and alanine release 11- to 17-fold at the start of reperfusion (P < .001). Furthermore, captopril increased myocardial oxygen and glucose uptake during reperfusion (P < .001 for both), whereas lactate release and myocardial blood flow were unaffected by captopril. At the start of reperfusion, there was a positive correlation between glutamate release and glucose uptake in captopril-treated hearts (r = 0.66, P = .05). We found no statistically significant differences between captopril and control hearts in tissue content of adenosine triphosphate, glycogen, glutamate, alanine, or lactate during 30 hours of cardioplegic storage.
Conclusions: The metabolic effects of captopril are strictly related to reperfusion, during which oxidative metabolism of glucose is improved. The captopril-induced increase in glutamate and alanine release at the start of reperfusion after cardioplegic storage may reflect a switch in metabolism of glucose-related amino acids.