Abstract
Ventricular myocardial cell action potentials were measuredin situ by means of intracellular microelectrodes in the heart of pyridoxine-deficient rats both at spontaneous frequency and at frequencies increased to higher levels. Pyridoxine deficiency lowered the rates of depolarization and repolarization phases of ventricular action potentials thus lengthening their duration. A noticeable bradycardia seemed to be induced by pyridoxine deficiency.
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