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F I Bonke

Publications and source records attributed to F I Bonke.

35 records · Page 2Linked to original sources
PubMed1976

The effect of heart rate on the membrane responsiveness of rabbit atrial muscle.

The maximum rate of rise of action potentials in myocardial fibers of the rabbit atrium decreases with an increase in heart rate. This decrease of the dV/dt max is accompanied by a decrease of the diastolic transmembrane potential prior to the moment of activation (take-off potential). Comparison of the membrane responsiveness curve (relation between dV/dt max and take-off potential) as measured by varying the extracellular potassium concentration at a fixed rate of stimulation, with the effect of changes in the frequency of stimulation on dV/dt max and take-off potential made clear that the fall in dV/dt max after a sudden increase in heart rate was stronger than could be explained by the concomitant decrease of the take-off potential alone. This implicates that the membrane responsiveness itself is heart rate dependent. A possible explanation for this observation is that when heart rate is increased the active Na/K pump is not able to maintain the intracellular concentration of Na and K at the original level. Acceleration of the heart will lead to an intracellular loss of potassium and a gain of sodium. The first causes a diminishment of the diastolic membrane potential which according to the membrane responsiveness curve is attended with a decrease of the dV/dt max. The second results in a decrease of the sodium concentration gradient and therefore in a further reduction of the dV/dt max. This hypothesis was confirmed by experiments with ouabain added to the perfusion fluid. Ouabain, which is known to inhibit the Na/K pump, caused a decrease of both the take-off potential and dV/dt max that was completely comparable with the effects of an increase of the frequency of stimulation. In addition, observation of the time course of the changes in dV/dt max and membrane "resting" potential after a sudden change in the rate of stimulation, gave support to the electrogenic concept of the active Na/K pump in cardiac muscle.

Action Potentials↗
PubMed1976

Circus movement in rabbit atrial muscle as a mechanism of tachycardia. II. The role of nonuniform recovery of excitability in the occurrence of unidirectional block, as studied with multiple microelectrodes.

Periods of tachycardia were induced in isolated segments (15 X 15 mm) of rabbit left atrium by local application of a properly timed premature stimulus. We used a special device for multiple synchronous microelectrode recordings of responses of more than 100 fibers during the initiation of tachycardia. We clearly demonstrated circus movement of the impulse through a small area of atrial muscle as the underlying mechanism. The premature impulse was conducted antegrade in only one direction, whereas in the other directions antegrade conduction failed. The local responses of the fibers in the blocked area served as a temporary obstacle for return of the premature impulse. When these fibers recovered their excitability before extinction of the premature impulse, they were reentered in a retrograde direction, and the impulse traveled in a circular route. During the propagation of a premature beat, local block, which set the stage for circus movement, was caused by nonuniform recovery of excitability of the atrium. We related the spread of activation of a premature impulse to the naturally occurring spatial dispersion in refractory periods and found that local conduction block invariably was associated with an area of delayed restoration of excitability. Artificial induction of differences in refractory periods by regional application of carbamylcholine made it clear that a disparity in refractory periods of only 11-6 msec between adjacent areas may be sufficient to cause local conduction block of a properly timed premature impulse.

Action Potentials↗
PubMed1975

The mechanism of supraventricular tachycardia induced by a single premature beat in the isolated left atrium of the rabbit. I. Circus movement as a consequence of unidirectional block of the premature impulse.

In the isolated left atrium of the rabbit tachycardia could be elicited by a single stimulus shortly after the refractory period. The activation pattern of the preparation was mapped by means of multiple extracellular recordings. It could be demonstrated that a circus movement of the activation in a relatively small part of the atrial myocardium was responsible for the tachycardia. This phenomenon was studied on a cellular level with multiple microelectrode recordings. The impulse of the premature beat, when followed by a tachycardia, was one way only, while in the other directions the conduction failed completely or occurred with such decrement that the impulse died out. These differences in conductivity were connected with spatial differences in the refractory period. Therefore the excitability of the fibers surrounding the stimulating electrod was not restored to the same level at the moment the premature beat was elicited. Spatial dispersion in the refractory period was important for the occurrence of unidirectional block and thus for the initiation of circus movement and tachycardia.

Action Potentials↗
PubMed1975

The mechanism of supraventricular tachycardia induced by a single premature beat in the isolated left atrium of the rabbit. II. The termination of the tachycardia.

Tachycardias induced by a single stimulus in the left atrium of the rabbit, are based on a circus movement of the impulse through the atrial myocardium. Circus movement often stopped spontaneously after only one beat ("coupled extrasystole") or after a small number of beats. This frequent early cessation of circus movement is explained by the relatively high conduction velocity and relatively long refractory period in the early stage of tachycardia. As an exception tachycardia lasted for a longer period. The circulating impulse then could always be interrupted by the application of a properly timed stimulus. In this case the circulating impulse will encounter the activation wave elicited by the stimulus. This resulted either in termination or resetting of the tachycardia.

Action Potentials↗
PubMed1975

Reentry in the atrium.

Studies with isolated atrial preparations of the rabbit showed that the occurrence of a single early premature beat may cause reentry not only in nodal tissue (SA node and AV node) but also in working myocardial tissue. In the SA node an early premature beat will cause a reentrant activation of the atrium only when the SA node is driven by an ectopic pacemaker. If the SA node is discharging spontaneously, no reentry could be demonstrated. In this situation the early impulse can not reach the center of the SA node because of a sinoatrial entrance block. Since the AV node fibers normally do not discharge spontaneously, an atrial premature beat may find an alternative route through the node and reenter the atrium. Such a reentrant beat or echo beat can start a tachycardia based on a circus movement of the impulse through the AV node. A supraventricular tachycardia can be started too by an early premature beat in the isolated left atrium, containing only working myocardial fibers and no slow conducting fibers as the nodal fibers are. By careful mapping the spread of activation during the premature beat and the subsequent beats of the tachycardia, a unidirectional block of the impulse of the premature beat was demonstrated. The impulse then turned around and invaded the blocked area retrogradely and reentered the area where it originated. This circus movement of the premature impulse was maintained during the subsequent tachycardial beats, showing that even in a small area of atrial muscle, containing no anatomical obstacle, a circus tachycardia can take place. To describe this kind of circus movement a new model (the "leading circle" concept) is introduced and briefly discussed.

Atrial Function↗
PubMedDate not supplied

Evidence for the presence of electrotonic depression of pacemakers in the rabbit atrioventricular node. The effects of uncoupling from the surrounding myocardium.

In the isolated AV junctional preparation of the rabbit heart, the presence of electrotonic influences on impulse formation was investigated. After disconnection of the sinus node, impulse formation started in the junctional area with a mean frequency of 72 beats/min (n = 17), which is about 40% of the sinus rate. Intracellular recordings were obtained to determine pacemaker location and activation sequence in the junctional area. The pacemaker was always located in the area of the lower nodal fibers of the AV node (thus distally from the site of maximal conduction delay) and these fibers had the highest rate of diastolic depolarization. Since it is known that pacemaker fibers are electronically influenced by their neighbouring cells, we investigated whether AV nodal automaticity was influenced by its surrounding tissue. Therefore the AV node was isolated from the atrial tissue and His bundle. This caused an enormous increase in diastolic depolarization rate, especially in the lower nodal fibers, accompanied by a rhythm acceleration to a mean of 137 beats/min. From the findings of the present study it was concluded that under normal conditions impulse formation in the lower nodal fibers of the rabbit AV node is electronically depressed by the connecting myocardium.

Action Potentials↗