Metabolism and the electrical activity of human atrial myocardium.

Abstract

The electrophysiological effects of hypoxia, glucose and iodoacetic acid (IAA) were studied in 16 preparations of human right atrial tissue obtained during corrective open heart surgery. During atrial pacing, transmembrane action potentials were recorded with intracellular micro-electrodes. Hypoxia caused predominant alterations in the repolarisation phase of the action potential including depression of the plateau and a decrease in duration associated with a shortening of the effective refractory period and an increase in the maximum atrial rate at which 1:1 conduction was still maintained. The maximum rate of rise was moderately reduced but the resting potential, action potential amplitude and conduction time were not significantly altered. The critical range of stimulus intervals at which inhomogeneity of conduction first occurred was shifted to shorter values. An increase in the extracellular glucose concentration from 5 to 50 mmol·litre−1 in the presence of persisting hypoxia reversed the anoxic effects. The action of IAA (7.5 × 10−5 mol·litre−1) alone on repolarisation resembled qualitatively that obtained with hypoxia but with a slower time course. The maximum rate of rise was not significantly altered. Combination of IAA with hypoxia rapidly abolished all atrial electrical activity. The results support the hypothesis that: (1) human atrial fibres can utilise both aerobic and glycolytic energy for maintenance of electrical activity; (2) under physiological extracellular glucose concentrations, either aerobic or glycolytic processes alone can provide sufficient energy to maintain the action potential amplitude but not the action potential plateau; and (3) stimulation of glycolysis by high extracellular glucose during hypoxia allows additional energy production that effectively contributes to the maintenance of the electrical activity of the human heart.