ABSTRACT
In experiments on dogs with acute left descending coronary artery occlusion, ethmozine (3 mg/kg) was tested for effects on the threshold of ventricular fibrillation occurring as a result of high-frequency electric stimulation. Two hours after occlusion, the fibrillation threshold became significantly lower than the control values. Ethmozine used in this period enhanced the ventricular fibrillation threshold in some experiments and diminished it in the others. Four hours following the occlusion, the fibrillation threshold did not differ from the control ones. Ethmozine given in this period caused a significant increase in the ventricular fibrillation threshold. It was concluded that 4 hours after the onset of experimental myocardial infarction are the minimal time period following which administration of ethmozine failed to decrease electric stability of the heart.
Subject(s)
Moricizine/therapeutic use , Myocardial Infarction/physiopathology , Ventricular Fibrillation/drug therapy , Animals , Dogs , Electric Stimulation , Female , Male , Moricizine/administration & dosage , Time Factors , Ventricular Fibrillation/etiologyABSTRACT
Experiments were made in dogs weighing 15-25 kg with experimental tourniquet shock (35 dogs) and experimental myocardial infarction (29 dogs). Intravenous injection of sodium thiosulfate (500 mg/kg) exerted a marked therapeutic effect on cardio- and central hemodynamics under acute circulatory disturbances both in tourniquet shock and myocardial infarction. Sodium thiosulfate increased cardiac discharge, minute blood flow volume, the first derivative, the threshold of ventricular fibrillation, improved the heart work, decreased and normalized the general peripheral resistance. This effect is likely to be related to the stimulation of intracellular metabolism and antidote action of sodium thiosulfate against ischemic toxin.