In the theory of electrocardiography the direction of myocardial fibers has been almost ignored. In order to evaluate whether this is proper or not, directional difference of conduction velocity in the ventricular syncytium was examined by capillary microelectrodes. Conduction velocity in the direction of myocardial fibers was found to be usually several times larger than that vertical to them. This difference is significantly large and cannot be ignored even though rapidity of conduction through Purkinje fibers is considered. This statement became more applicable in various abnormal conditions. Thus it is concluded that the direction of myocardial fibers should be given more attention in discussion of propagation of excitation waves in the cardiac ventricle.
Microelectrodes were employed to determine the mode of propagation of excitation from the sinus node in the rabbit heart. The excitation starts from the sinus node radially, at first, but then proceeds to the crista terminalis, often obliquely. This is because some special tissue having a slow conduction velocity lies behind the sinus node, and also because there is a zone of relatively faster conduction at the basal wall of the superior vena cava. Once the excitation wave enters the crista terminalis, it travels rapidly in two opposite directions through two branches of the ring-like structure which is formed by the crista terminalis and its extension. The excitation wave traveling through the branch encircling the inferior vena cava reached the atrioventricular node earlier in most instances.
In the caval region inside the ring-like structure there is a zone of relatively faster conduction. The conduction to the atrioventricular node through this route is latent in the normal state, because conduction through the ring-like structure takes place beforehand.
In the caval region near the sinus node, the conduction velocity of the excitation wave from the spontaneously beating sinus node was greater than that from the electrically driven atrium. The spontaneous action potential showed also a steeper rise than that produced by electrical stimulation. The mechanism responsible for this is discussed.
The isolated rabbit sinus node was partly divided into two parts by a cut in the middle portion. Microelectrode recording near the bridge connecting the two parts revealed an interference between action potentials from the two parts. Comparison of microelectrode recordings from the two parts taken near the bridge suggested that an induced peculiar rhythm change in one part was probably induced by the electrotonic effects of the action potentials of the other part. To prove this, a subthreshold depolarizing square-wave pulse was applied extracellularly to the isolated uncut sinus node. When the pulse was applied in the early portion of slow diastolic depolarization, diastole was prolonged, and when it was applied in the later portion, diastole was shortened. These findings can explain the observed peculiar thythm and suggest that in the mammalian sinus node, pacemaker cells accelerate or decelerate mutually by the electrotonic effects of their action potentials, depending on the phase of application of the effects. In particular, for some time the faster pacemaker cells could be influenced by dragging effects from the neighboring slower pacemaker cells and the slower pacemaker cells by pulling effects from the neighboring faster pacemaker cells.
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