COENZYME-Q(10) PROTECTS ISCHEMIC MYOCARDIUM IN AN OPEN-CHEST SWINE MODEL

Myocardial stunning, defined as a reversible decrease in contractility after ischemia and reperfusion, may be a manifestation of reperfusion injury caused by free oxygen radical damage. The aim of this study wa s to test the hypothesis that pretreatment with coenzyme Q10 (ubiquino ne), believed to act as a free radical scavenger, reduces myocardial s tunning in a porcine model. Twelve swine were randomized to receive ei ther oral supplementation with coenzyme Q10 or placebo for 20 days. A normothermic open-chest model was used with short occlusion (8 min) of the distal left descending coronary artery followed by reperfusion. R egional contractile function was measured with epicardial Doppler crys tals in ischemic and nonischemic segments by measuring thickening frac tion of the left ventricular wall during systole. Stunning time was de fined as the elapsed time of reduced contractility until return to bas eline. Coenzyme Q10 concentrations were measured in blood and homogeni zed myocardial tissue by high performance liquid chromatography. Plasm a levels of reduced coenzyme Q10 (ubiquinol) were higher in swine pret reated with the experimental medication as compared to placebo (mean 0 .45 mg/l versus 0.11 mg/l, respectively). Myocardial tissue concentrat ions, however, did not show any changes (mean 0.79 mug/mg dry weight v ersus 0.74 mug/mg). Stunning time was significantly reduced in coenzym e Q10 pretreated animals (13.7+/-7.7 min versus 32.8+/-3.1 min, P < 0. 01). In conclusion, chronic pretreatment with coenzyme Q10 protects is chemic myocardium in an open-chest swine model. The beneficial effect of coenzyme Q10 on myocardial stunning may be due to protection from f ree radical mediated reperfusion injury. This protective effect seems to be generated by a humoral rather than intracellular mechanism.