Some of the relationships between metabolism, membrane potentials and contractility in cardiac tissue have emerged from a study of the effects of anoxia, depletion of substrate and dinitrophenol on the rat atrium. The repolarization phase of the action potential was shown to be particularly sensitive to disturbances in metabolism. Depression of metabolism resulted in a more rapid repolarization, which may provisionally be interpreted as an acceleration of K + efflux; restoration of metabolism reversed this effect. A concept relating membrane potentials and metabolism is presented, involving the presence of bound ATP within the membrane.

Acetylcholine diminished the developed tension of contraction in rat atria; simultaneously there was a slight increase in resting potential, no appreciable change in action potential, a decrease in the rate of conduction, only a minor alteration of the form of contraction, and, most strikingly, a decrease in the duration of the action potential or the area enclosed by it. The rate of repolarization subsequent to the action potential was markedly accelerated. Epinephrine, in general, produced the opposite effects and slowed the repolarization rate as it augmented atrial contraction. Cholinesterase does not seem to play a direct role in cardiac membrane potentials or ion transfer since physostigmine had no effect of its own on the electric manifestations. Certain aspects of the mechanisms involved are discussed.

Simultaneous recording of membrane potentials and contractility in isolated rat atria by means of intracellular micro-electrodes and a sensitive strain gage has been used to establish the normal characteristics of the tissue as well as effects of temperature, stimulus frequency and initial tension on muscle. Preliminary correlations between duration of the action potential and the degree of contraction indicate that the rate of repolarization is of major importance in determination of the contractile response. IT is generally believed that the contraction of a muscle cell is initiated by the membrane depolarization of the propagated action potential, but no exact quantitative formulation has been made whereby the degree of tension can be related to the various characteristics of the depolarization process. Before the coupling between excitation and contraction can be quantitatively expressed and the mechanism of this coupling elucidated, such accurate relationships must be established. The present report will be concerned with the membrane electric characteristics and contractile properties of the rat atrium, and the effects of variation of several factors on the depolarization and repolarization processes as related to the contractile tension. The use of intracellular microelectrodes allows an accurate determination of membrane potentials and their variations, but for the correlation with contractility it is necessary to record simultaneously the tension changes; such an apparatus has been designed and is similar to that described by Burgen and Terroux 1 . It is believed that after a quantitative correlation is made between membrane potential changes and contractility and the metabolic basis for these processes From the

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A new method of evoked response detection, previously demonstrated in the ventricle, has been studied in the atrium at the time of routine pacemaker implant in 16 patients. The atrial evoked response was readily detectable in all patients due to excellent recovery from poststimulus polarization. In six patients, as experimental threshold-tracking pacemaker was used to automatically verify atrial capture and to generate strength-duration curves. It is concluded that this pacing technique is both simple and reliable, and that automatic atrial threshold tracking is feasible.