Аннотация:Objective: Acute myocardial infarction (MI) is accompanied by significant inflammation following tissue necrosis especially pronounced on the 3rd day. Coenzyme Q10 (CoQ10) is a potent antioxidant and putative modulator of inflammation. Intravenous (i.v.) CoQ10 administration leads to rapid elevation of myocardial CoQ10 levels. The aim of the present study was to study effects of CoQ10 injected i.v. after coronary occlusion on the size of the postinfarction inflammation zone.
Design and Methods: The experiments were carried out on the rat model of acute MI induced by coronary artery ligation. Solubilized CoQ10 (30 mg/kg) was administered i.v. in 10 min after occlusion. Control infarct rats received saline. 3 groups of rats were compared: MI-saline (n=7), MI-CoQ10 (n=8) and Sham-operated-saline (n=7). Severity of the myocardium damage, CoQ10 tissue levels were evaluated on the 3rd day after coronary occlusion. Cuts of myocardium were stained by hematoxyline/eosine and studied by microscopy (Leica DM 4000) using Leica Application Suite 8.0 software. The size of necrosis zone and infiltration zone was estimated as ratio of theirs area to total slice area. The CoQ10 content was measured by HPLC with electrochemical detection. Statistical analysis was performed using Mann-Whitney U-test.
Results: In 3rd day after operation the control infarct rats had extensive transmural myocardial necrosis. In MI-CoQ10 group 7 from 8 rats had foci of necrosis observed within the left ventricle wall. In MI-CoQ10 group the smaller zone of damage (necrosis area plus infiltration area) was observed (18.4%) in comparison with MI-saline group (42%, p<0.001). Both of areas were expressed lesser in MI-CoQ10 group as compared with MI-saline group (2.7% vs 15.7% and 14.8% vs 27.2% correspondently, p<0.001). In 3rd day after CoQ10 injection its plasma level was increased 25-fold (p<0.01) when compared with the control infarct rats.
Conclusion: Single i.v. administration of CoQ10 after acute MI protects the cardiac tissue against non-reversible regional ischemia reducing the necrosis and the size of the inflammation zone.