Abstract
Prevention of chloroform-induced ventricular fibrillation has been the basis of an antiarrhythmic screening technique in mice. However, data from this laboratory indicated that exposure of mice to chloroform evokes ventricular tachycardia rather than ventricular fibrillation. In view of these observations, the original screening technique was revised and new criteria for antiarrhythmic activity were established. Subsequent validation of those criteria was determined with various beta antagonists and Class I antiarrhythmic agents. Each group of agents evoked dose-dependent antiarrhythmic activity whereas most Class I agents also evoked ataxia which was presumed to be of CNS origin. The revised screening procedure appears to be a sensitive and reliable predictor of antiarrhythmic activity and also provides information regarding the potential for undesirable CNS side effects.
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