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

Objective: We sought to evaluate the effects of captopril on glucose-relate d metabolism during hypothermic cardioplegic storage and subsequent reperfu sion. Methods: We compared hearts from control Digs with hearts from pigs treated with increasing oral doses of captopril for 3 weeks (12.5-150 mg daily), a n intravenous bolus (25 mg) before operation, and captopril-containing card ioplegic solution (1 mg/L). The hearts were excised after infusion of cold crystalloid cardioplegic solution and stored ill saline solution (4 degrees C-6 degrees C). In one series we studied myocardial blood now and arteriov enous differences in oxygen, glucose, lactate, glutamate, and alanine durin g 60 minutes of postcardioplegic blood reperfusion. In this series captapri l-treated heal ts were reperfused with captopril-containing blood(1 mg/L), In another series we obtained biopsy specimens from the left ventricle thro ughout 30 hours of hypothermic cardioplegic storage and monitored tissue co ntent of energy-rich phosphates, glycogen, glutamate, and alanine. Results: Captopril increased glutamate and alanine release 11- to 17-fold a t the start of reperfusion (P < .001). Furthermore, captopril increased myo cardial oxygen and glucose uptake during reperfusion (P < .001 for both), w hereas lactate release and myocardial blood flow were unaffected by captopr il. At the start of reperfusion, there was a positive correlation between g lutamate release and glucose uptake in captopril-treated hearts (r = 0.66, P = .05). We found no statistically significant differences between captopr il 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 rep erfusion, during which oxidative metabolism of glucose is improved. The cap topril-induced increase in glutamate and alanine release at the start of re pel fusion after cardioplegic storage may reflect a switch in metabolism of glucose-related amino acids.