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Single Intravenous Injection of CoQ10 Reduces Infarct Size in a Rat Model of Ischemia and Reperfusion Injury

Myocardial infarct, commonly known as a heart attack, occurs when blood flow decreases or stops to a part of the heart, causing irreversible loss of cardimyocytes accompanied by deterioration of contractile function and arrhythmias. Maintenance of mitochondrial activity and antioxidant features of coenzyme Q10 (CoQ10) could be an effective background for treatment of acute myocardial ischemia. Dietary uptake of CoQ10 is limited to only a few percent. In urgent cases, parenteral administration of CoQ10 could provide fast increase of its plasma and myocardial levels. The aim of the study is to investigate the effects of single intravenous (i.v.) pretreatment of solubilized CoQ10 on its myocardial level and IR injury.

30 min prior to coronary artery occlusion rats received i.v. solubilized CoQ10 (30 mg/kg) or saline (1 ml/kg). After 30 min of ischemia and 120 min of reperfusion, infarct zone of left ventricle (LV) and quantity of CoQ10 in LV were determined. Cardiac rhythm was monitored through the whole experiment. The results indicated that at the beginning of reperfusion, arrhythmias were recorded in 8 (from 9) in saline and 2 (from 9) in CoQ10-treated rats. Arrhythmias in CoQ10-treated rats arose later (40 ± 8 sec) and had less duration (26 ± 14 sec); 14 ± 13 sec and 52 ± 17 sec in saline treated rats respectively. At the end of reperfusion CoQ10 treated rats revealed: 2 fold higher CoQ10 content in LV (p < 0.01), limitation of infarct zone by 35% (p < 0.01). Higher levels of CoQ10 were accompanied by less infarct size (r = 0.77, p < 0.001).

In conclusion, single i.v. injection of CoQ10 effectively increased its myocardial levels and protected heart against IR injury by diminishing the size of the irreversibly damaged myocardium, decreasing frequency and duration of arrhythmias. The infarct zone inversely correlated with the quantity of CoQ10 in LV.

Article by Alexander Ivanov, et al, from Russia.

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