ON THE MODE OF ACTION OF GLUCOSE IN THE MAINTENANCE OF VENTRICULAR FIBRILLATION

Abstract

Glucose deprivation was previously shown to favor the induction of ventricular fibrillation in the isolated and perfused rabbit heart. On the other hand, glucose is required for the prolonged maintenance of the induced fibrillation.The mechanism of action of glucose in the maintenance of electrically induced fibrillation was studied in 54 hearts perfused with solutions containing either normal or decreased sources of available energy. Hearts perfused with a normal solution, a low-sucrose solution, or with a glucose-free solution containing lactate or adenosine-triphosphate develop long-lasting fibrillations.It is believed that glucose deprivation acts, initially, by inhibiting the active cardiac mechanism delaying repolarization and by reducing, therefore, the duration of the action potential and rendering the heart more vulnerable to fibrillatory factors. During a second phase, brought about by a decrease in the effectiveness of the sodium pump and by a shift in the sodium and potassium fluxes, glucose deprivation lengthens the duration of the action potential and refractory period and produces an antifibrillatory effect. Dinitrophenol is thought to act in a similar manner, but the fibrillatory action of adenosine triphosphate cannot be explained as satisfactorily.