ABSTRACT
The experiments with models of myocardial infarction established that carnitine chloride reduced the size of an ischemic zone, prevented oxidative metabolism, lowered ATP and creatine phosphate levels, inhibited lactate and free fatty acid accumulation in the ischemic myocardium. Carnitine chloride in combination with nitrong and isoptin increased the anti-ischemic potency of the former.
Subject(s)
Carnitine/therapeutic use , Myocardial Infarction/drug therapy , Animals , Carnitine/administration & dosage , Cats , Clinical Enzyme Tests , Drug Therapy, Combination , Myocardial Infarction/diagnosis , Myocardial Infarction/metabolism , Myocardium/metabolism , Nitroglycerin/administration & dosage , Nitroglycerin/therapeutic use , Rats , Rats, Inbred Strains , Verapamil/administration & dosage , Verapamil/therapeutic useABSTRACT
The antiarrhythmic activity of quinasopirine was studied in the experiments on rats with the use of models of calcium chloride- and aconitine-induced arrhythmias, disorders of cardiac rhythm in myocardial infarction produced by isadrine and pituitrin and also in the experiments on cats in arrhythmias caused by electric stimulation of the myocardium, postinfarction and reperfusion arrhythmias. Quinasopirine exhibits the antiarrhythmic effect being superior to that of anapriline and novocainamide in arrhythmias induced by calcium chloride and aconitine. In other types of the cardiac rhythm disorder its activity is comparable with that of ethmosine, obsidane and cordarone. Quinasopirine reduces automatism and contractile function of the myocardium.