The passive electrical properties of neonatal rat heart cells grown in monolayer cultures were determined. Hyperpolarizing current pulses were injected through one microelectrode via an active bridge circuit. Membrane voltage displacements caused by the injected current pulses were measured at various distances from the first with a second microelectrode. Using a modified least-squares method the experimental results were fitted to a Bessel function, which is the steady-state solution of the differential equation describing the relation between membrane voltage caused by current injection and interelectrode distance in a very large and very thin plane cell. Best fit was obtained with a space constant of 360 μm and an internal resistivity of 500 Ω cm. From these figures, specific membrane resistance was calculated to be 1,300 Ω cm(2), assuming all current to leave through the upper surface of the monolayer.The time constant of the membrane was measured from the time course of the current-induced membrane voltage displacements. From its value of 1.7 msec a membrane capacity of 1.3 μF/cm(2) was calculated.From these results and some literature data on nexus distribution (A. W. Spira,J. Ultrastruct. Res. 34:409, 1971) specific nexus resistance was calculated to range between 0.25 and 1.25 Ω cm(2), depending on the amount of folding of the intercalated discs. The results suggest that spread of activation in monolayer cultures of heart cells by means of local circuit currents is very likely.
In the isolated right atrium of the rabbit, premature beats were elicited by electrical stimulation. When the activation front of a premature beat did not reach the sinoatrial (S-A) node soon enough to discharge the pacemaker prematurely, the pause following the premature beat was compensatory. However, when the activation front forced the pacemaker to discharge prematurely, the premature beat cycle outlasted the normal spontaneous pause, although it was not completely compensatory. Moreover, several cycles after the premature beat were prolonged. The postextrasystolic pause lasted longer if the premature beat was elicited earlier in the atrial cycle. Several changes in the activity of the S-A node caused the prolonged diastole after the atrial premature beat; the most prominent change was a pacemaker shift that persisted several cycles after the premature beat. We found a progressive decrease of the conduction velocity within the S-A node when the latency between the spontaneous discharge of the pacemaker and the arrival of the premature impulse from the atrium in the S-A node was shortened. This may explain the occurrence within the S-A node of a shift of the pacemaker in the direction of the ectopic focus. The rhythm of the new pacemaker was slower than that of the original one. ADDITIONAL KEY WORDS diastolic depolarization pacemaker shift conduction velocityS-A node postextrasystolic pause automaticity compensatory pause transmembrane potentials stimulation• If an impulse originating from an atrial ectopic focus does not reach the sinoatrial (S-A) node before its spontaneous discharge, the lengthening of the interval after the premature beat is fully compensatory. The premature beat inhibits the conduction of the spontaneous impulse from the nodal pacemaker over the atrium. Only the next spontaneous impulse is conducted and activates the atrium. If, on the contrary, the impulse from the ectopic focus forces the pacemaker to discharge prematurely (1), the regularity of the pacemaker will be disturbed and the postextrasystolic pause will be too short to be compensatory, although longer than the normal interval. The postextrasystolic pause lengthens proFrom the Department of Physiology, University of Amsterdam, Amsterdam, The Netherlands.Received December 26, 1968. Accepted for publication February 15, 1969. gressively as the premature beat is elicited earlier in the atrial cycle, i.e., as the curtailed cycle is shorter. To explain this phenomenon, Wenckebach supposed that the conduction velocity of the impulse from an ectopic focus is less as the curtailed cycle is shorter. Eccles and Hoff (2) assumed that a temporary depression of rhythmicity also occurs.Since then, the factors determining the duration of the postextrasystolic pause have not been investigated. In the experiments presented here, we elicited premature beats in the atrium and in the S-A node by electrical stimulation and turned our attention to:(1) The relation between the durations of the curtailed cycle and postextrasystolic pause.(...
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