Creatine phosphate suppresses ventricular arrhythmias resulting from coronary artery ligation.
The effects of various doses of creatine phosphate have been examined in a rat model of acute myocardial ischaemia. When given directly into the lumen of the left ventricle in pentobarbitone-anaesthetised male rats, creatine phosphate (50 and 100 mg/kg) markedly reduced the incidence of ventricular ectopic beats, and especially the incidence and duration of ventricular tachycardia and fibrillation which normally resulted from acute coronary artery ligation in this model. This protection was observed even if 1 of 2 h elapsed between creatine phosphate administration and coronary artery ligation. Electrophysiological studies on papillary muscles removed from rats 1 h after administration showed that creatine phosphate both decreased the maximum rate of depolarisation and prolonged the duration of the action potential. These results confirm our previous work in dogs that creatine phosphate is effective against early postinfarction ventricular arrhythmias, at least if given locally. It is suggested that these effects are due, at least in part, to a prolongation of the cardiac muscle action potential. Whether this is the result of maintaining energy production early in myocardial ischaemia is unclear.
D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001145:Arrhythmias, Cardiac / Q000517:prevention & control*; D003327:Coronary Disease / Q000150:complications* / Q000503:physiopathology; D006321:Heart / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D008297:Male; D010210:Papillary Muscles / Q000502:physiology; D010725:Phosphocreatine / Q000494:pharmacology*; D051381:Rats
D010725:Phosphocreatine