Influence of uidine on miocardium energy metabolism, lipid peroxidation and antioxidant system in acute coronary deficiency. Role the mitochondrial ATP-sensitive K+-channel.

Earlier we demonstrated that uridine-5’-diphosphate (UDP) possess the property to activate mitochondrial ATP-dependent K+-channel (mitoKATP). Now we have found that UDP precursors - uridine at a concentration of 30 mg/kg stabilized oxidative and energy metabolism of heart after 60 minute left coronary artery occlusion. Uridine administration restored ATP and creatine phosphate levels, which were decreased after occlusion of the left coronary artery. Deficiency of energy compounds in rat ischemic myocardium was accompanied by a significant increase in the amount of lipid hydroperoxide (97%), decrease in activity of SOD by 28% and reducing the amount of reduced glutathione by 30%. In the serum, activity of paraoksanase – еnzyme, exhibiting antioxidant and anti-atherogenic properties by preventing the oxidation of lipids, was increased by 93%. Selective inhibitor of mitoKATP 5-hydroxydecanoate prevented the protective effect of uridine. This data are in agreement with our previously results that uridine possess anti-ischemic and anti-arrhythmic effects, namely can reduce zone of ischemia, the amplitude of T-wave on ECG, and decrease heart rhythm disturbances on the model of acute myocardial infarction. The data allow us to conclude that mitoKATP is involved in the cardioprotective mechanisms of uridine action.