Cellular Membrane Potentials and Contractility of Normal Rat Atrium and the Effects of Temperature, Tension and Stimulus Frequency

Abstract

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

Anoxia and Ventricular Fibrillation; With a Summary of Evidence on the Cause of Fibrillation

“…They found that in the range 38-19', the action potential, particularly the plateau, became longer as the temperature fell. The same observation was also made by Hollander and Webb (1955). Marshall (1957) observed the same change in the transmembrane potential of single fibres of the rabbit atrium; the duration of the action potential rose from 240 msec.…”

The effect of increased filling pressure on rhythmicity and atrioventricular conduction in isolated hearts

“…The later depressive effect of high filling pressures may be related to the fact that substantial lowering of the membrane potential reduces the availability of the sodium-carrying 'spike' mechanism (Weidmann, 1955). Although neither Dudel & Trautwein (1954) nor Hollander & Webb (1955) were able to detect any change in the height or duration of the cardiac action potential on moderate stretching, the observation of the former authors that the action potential of Purkinje fibres was diminished by excessive stretching is in keeping with this view. Such effects might well appear earlier in normal and abnormal pace-makers which must depolarize spontaneously at a more rapid rate than other cardiac muscle cells.…”

Length-dependent changes of pacemaker frequency in the isolated rabbit sinoatrial node.

“…It has long been known that distension of mammalian atrial tissues including the sinoatrial (SA) node produces an acceleration of heart rate (BAINBRIDGE,1915;SASSA and MIYAZAKI, 1920;SCHERF et al, 1949;HOLLANDER and WEBS, 1955;BLINKS, 1956;PATHAK, 1959) which appears to be due to a direct action on the pacemaker cells. Brooks and his coworkers LANGE et al, 1966) studied the effect of stretch on the discharge rate of in situ or isolated mammalian SA nodal region and suggested that the stretch-induced acceleration of pacemaker activity is mediated by a lowering of membrane potential caused by an increase in Na permeability, while extrinsic nerves are not essential to this reaction.…”