Abstract
Summary
Evidence is presented to demonstrate that quinidine, when administered as described here, produces a significant and progressive hypopotassemia; with a non-significant variation in the arteriovenous potassium concentration, denoting that the drug does not alter the normal efflux or influx of the potassium ion at the somatic muscle cell level. The drug also effects a marked hyperglycemia and an apparent inhibition of K transport at the gut level. The electrocardiographic evidence suggests the possibility that the mechanism of action of quinidine may be directly related to the latter's effect on the potassium ion.
Thanks are due to Dr. Roger M. Reinecke for valuable advice.
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