Beneficial effect of coenzyme Q on myocardial slow action potentials in hearts subjected to decreased perfusion pressure—hypoxia—substrate-free perfusion

Summary

Coenzyme Q, an important component of the electron transfer system in mitochondria, plays a central role in energy production aerobically. The effect of pretreatment with coenzyme Q₁₀ (Co Q) on myocardial slow action potentials (APs) and accompanying contractions and on myocardial high energy phosphate content was studied in perfused hearts subjected to decreased perfusion pressure—hypoxia—substrate-free. Post-hatched chicks were treated i.p. with 10 mg/kg of Co Q daily for 5 days. To study the slow APs exclusively, the fast Na⁺ channels were voltage-inactivated by elevated K⁺ (25 mM) Tyrode solution. The Ca⁺⁺-dependent slow APs were induced by elevating [Ca]₀ to 5.4 mM; hearts were paced at a rate of 40 per min. Hearts which had been pretreated with Co Q were protected against the deleterious effect of decreased perfusion pressure—hypoxia—substrate-free perfusion on mechanical performance accompanying the slow Ca⁺⁺−Na⁺ APs. The slow APs in hearts pretreated with Co Q were also less affected than were non-treated hearts. However, the myocardial ATP and total adenine nucleotides were not affected by exogenous Co Q. It was suggested that exogenous Co Q could protect against the decline of cardiac contractions via improved availability of slow APs during decreased perfusion pressure—hypoxia—substrate-free, independently of the cellular high energy phosphate level.