Abstract
SC-7031 was effective at approximately ½ to ⅓ the effective dose of quinidine against certain cardiac arrhythmias in the dog. Atrial arrhythmias were reverted by intravenous closes of 5.8 ± 0.9 mg/kg (9 dogs) when induced electrically, and by 2.7 ± 0.5 mg/kg (10 dogs) when caused by local application of aconitine nitrate. Oral dosage was effective at about 15 mg/kg in both procedures. SC-7031 in intravenous doses of 3 and 5 mg/kg (4 dogs) corrected the abnormal electrocardiogram obtained with experimental coronary occlusion. Oral closes of 20 mg/kg were effective in 2 such dogs. In 3 ouabain-intoxicated dogs, SC-7031 corrected the ventricular tachycardia when given in intravenous doses of 15, 10, and 10 mg/kg. There was depression of cardiac output, but no significant change in blood pressure after SC-7031 in anesthetized dogs. No data on these parameters were obtained from conscious animals. SC-7031 blocked the cardiac vagus nerve but had no effect on sympathetic nervous function. Acute toxicity was relatively low, the intravenous therapeutic ratio in clogs being about 10. These data suggest that SC-7031 may be more potent and dependable than quinidine and procaine amide in the treatment of certain clinical arrhythmias of the atrium and ventricle.
Footnotes
- Received August 17, 1961.
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