Beneficial effect of coenzyme Q on myocardial slow action potentials in hearts subjected to decreased perfusion pressure-hypoxia-substrate-free perfusion.
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]o 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.
D000818:Animals; D002645:Chickens; D003326:Coronary Circulation / Q000187:drug effects*; D003327:Coronary Disease / Q000188:drug therapy*; D004562:Electrocardiography; D004579:Electron Transport / Q000187:drug effects; D006329:Heart Conduction System / Q000187:drug effects; D009200:Myocardial Contraction / Q000187:drug effects; D010101:Oxygen Consumption / Q000187:drug effects*; D010477:Perfusion; D014451:Ubiquinone / Q000494:pharmacology*
D014451:Ubiquinone