Abstract

Experiments were undertaken to determine if pretreating the animal with coenzyme Q 10 (CoQ) protected the cardiac muscle of the isolated perfused heart which was exposed to global ischemia for 30 min and then reperfusion. Two hours after the intramuscular (20 mg/kg) and intraperitoneal (10 mg/kg) injections of CoQ or vehicle alone the hearts were excised and perfused by Langendorff's technique. In the vehicle-pretreated group, ischemia caused a precipitous decline of the contractile tension development, an elevation of the resting tension and a severe contracture. During the substrate-free reperfusion for 30 min, there was a small decrease in the magnitude (25%) of the contracture, and, yet, no tension development. In the additional reperfusion with glucose as the substrate for 30 min, the tension development was slightly (11%) recovered. Tissue ATP and total adenine nucleotide contents at the end of the glucosereperfusion markedly decreased. Although pretreatment with CoQ had no effect on the onset and progression of ischemic contracture, it facilitated the recovery of mechanical performance. Cardiac stores of both ATP and total adenine nucleotide in CoQ-pretreated reperfused hearts were significantly ( P < 0.01) higher than those in vehicle-pretreated group. There was a direct relation between the extent of the recovery of mechanical performance and tissue ATP content. It was suggested that exogenous CoQ protected the cardiac muscle from the deterioration of mechanical function of ischemia and recovery. Better mechanical function of CoQ-pretreated heart was attributable to better resynthesis of ATP presumably due to lesser loss of adenine nucleotide pool from the cardiac cells.

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