Delayed Myocardial Metabolic Recovery After Blood Cardioplegia

• Published in: The Annals of thoracic surgery Vol. 48; no. 4; pp. 503 - 507
• Main Authors: Weisel, Richard D., Mickle, Donald A.G., Finkle, Carolyn D., Tumiati, Laura C., Madonik, M. Mindy, Ivanov, Joan
• Format: Journal Article
• Language: English
• Published: New York, NY Elsevier Inc 01-10-1989; Elsevier Science
• Subjects: Adenosine Diphosphate - metabolism; Adenosine Monophosphate - metabolism; Adenosine Triphosphate - metabolism; Biological and medical sciences; Blood; Body Temperature; Chromatography, High Pressure Liquid; Coronary Artery Bypass - methods; Coronary Disease - surgery; Heart Arrest, Induced - methods; Humans; Hypoxanthine; Hypoxanthines - metabolism; Medical sciences; Middle Aged; Myocardium - metabolism; Phosphocreatine - metabolism; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases; Surgery of the heart; Time Factors; Uric Acid - metabolism; Human; Cardioplegic solution; Cardiac performance; Energy metabolism; Pathophysiology; Cardiovascular disease; Exploration; Treatment; Aortocoronary; Bypass; Surgery; Myocardium; Resuscitation
• ISSN: 0003-4975; 1552-6259
• DOI: 10.1016/S0003-4975(10)66850-6

Previous studies have demonstrated that both myocardial metabolism and ventricular function were depressed after blood cardioplegic arrest for elective coronary artery bypass grafting. To evaluate the etiology of this metabolic defect, we measured the levels of adenine nucleotides and their precursors in 29 patients undergoing elective coronary revascularization. Myocardial biopsy specimens were obtained at 37°C before cardioplegic arrest, immediately after 74 ± 4 minutes of cardioplegic arrest, and after 30 minutes of reperfusion. Biopsy specimens were analyzed for levels of adenine nucleotides and their precursors by high-performance liquid chromatography. Adenosine triphosphate concentrations decreased with cardioplegic arrest and with reperfusion. Adenosine monophosphate concentiations increased after cardioplegic arrest and remained nearly twice the initial values after reperfusion. The ratio of adenosine monophosphate to adenosine triphosphate doubled after reperfusion, suggesting defective conversion of adenosine monophosphate to adenosine triphosphate. Levels of adenine nucleotide degradation products (adenosine, inosine, and hypoxanthine) increased after cardioplegia and decreased with reperfusion, suggesting a washout of soluble precursors. This study suggests that improvements in myocardial protection should attempt to stimulate mitochondrial energy production and preserve adenine nucleotide precursors.