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J Thorac Cardiovasc Surg 1996;111:443-450
© 1996 Mosby, Inc.

CARDIOPULMONARY BYPASS, MYOCARDIAL MANAGEMENT, AND SUPPORT TECHNIQUES

ELUCIDATION OF A TRIPARTITE MECHANISM UNDERLYING THE IMPROVEMENT IN CARDIAC TOLERANCE TO ISCHEMIA BY COENZYME Q₁₀ PRETREATMENT

Philadelphia, Pa., and Copenhagen, Denmark

Supported by the National Institutes of Health grant HL 42922.

Address for reprints: Juan A. Crestanello, MD, Division of Cardiothoracic Surgery, The Medical College of Pennsylvania, 3300 Henry Ave., Philadelphia, PA 19129.

Abstract

Coenzyme Q₁₀, which is involved in mitochondrial adenosine triphosphate production, is also a powerful antioxidant. We hypothesize that coenzyme Q₁₀ pretreatment protects myocardium from ischemia reperfusion injury both by its ability to increase aerobic energy production and by protecting creatine kinase from oxidative inactivation during reperfusion. Isolated hearts (six per group) from rats pretreated with either coenzyme Q₁₀, 20 mg/kg intramuscularly and 10 mg/kg intraperitoneally (treatment) or vehicle only (control) 24 and 2 hours before the experiment were subjected to 15 minutes of equilibration, 25 minutes of ischemia, and 40 minutes of reperfusion. Developed pressure, contractility, compliance, myocardial oxygen consumption, and myocardial aerobic efficiency were measured. Phosphorus 31 nuclear magnetic resonance (³¹P-NMR) spectroscopy was used to determine adenosine triphosphate and phosphocreatine concentrations as a percentage of a methylene diphosphonic acid standard. Hearts were assayed for myocardial coenzyme Q₁₀ and myocardial creatine kinase activity at end equilibration and at reperfusion. Treated hearts showed higher myocardial coenzyme Q₁₀ levels (133 ± 5µg/gm ventricle versus 117 ± 4µg/gm ventricle, p < 0.05). Developed pressure at end reperfusion was 62% ± 2% of equilibration in treatment group versus 37% ± 2% in control group, p < 0.005. Preischemic myocardial aerobic efficiency was preserved during reperfusion in treatment group (0.84 ± 0.08 mm Hg/(µl O₂/min/gm ventricle) vs 1.00 ± 0.08 mm Hg/(µl O₂/min/gm ventricle) at equilibration, p = not significant), whereas in the control group it fell to 0.62 ± 0.07 mm Hg/(µl O₂/min/gm ventricle, p < 0.05 vs equilibration and vs the treatment group at reperfusion. Treated hearts showed higher adenosine triphosphate and phosphocreatine levels during both equilibration (adenosine triphosphate 49% ± 2% for the treatment group vs 33% ± 3% in the control group, p < 0.005; phosphocreatine 49% ± 3% in the treatment group vs 35% ± 3% in the control group, p < 0.005) and reperfusion (adenosine triphosphate 18% ± 3% in the treatment group vs 11% ± 2% in the control group, CTRL p < 0.05; phosphocreatine 45% ± 2% in the treatment group vs 23% ± 3% in the control group, p < 0.005). Creatine kinase activity in treated hearts at end reperfusion was 74% ± 3% of equilibration activity vs 65% ± 2% in the control group, p < 0.05). Coenzyme Q₁₀ pretreatment improves myocardial function after ischemia and reperfusion. This results from a tripartite effect: (1) higher concentration of adenosine triphosphate and phosphocreatine, initially and during reperfusion, (2) improved myocardial aerobic efficiency during reperfusion, and (3) protection of creatine kinase from oxidative inactivation during reperfusion. (J THORAC CARDIOVASC SURG 1996;111:443-50)

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