Ventricular fibrillation is not an anodally induced phenomenon in open-chest dogs

It is generally assumed that ventricular fibrillation evoked by electrical stimulation depends on anodal excitation. To test this hypothesis, six open-chest dogs were studied with computerized mapping techniques. A plaque electrode array containing 56 closely (2.5-5 mm) spaced bipolar electrodes was placed on the right ventricle. The patterns of activation after premature stimulation and at the onset of multiple responses or ventricular fibrillation were determined when the baseline driving stimuli (S1) were given to the center, and when a 5-ms bipolar single premature stimulus (S2) was given via two electrodes (one anodal and one cathodal) at the opposite edges of the plaque electrode array. The results showed that the classical anodal and cathodal strength-interval curves could be demonstrated by this method. A relatively supernormal period was observed only in the anodal strength-interval curve and coincided with the most vulnerable phase of the cardiac cycle. Although a supernormal period was found only at the anodal site, the origins of excitation at the onset of multiple responses or ventricular fibrillation could be anodal, cathodal, or both. When the S2 polarity was reversed, the origin of multiple responses or ventricular fibrillation stayed at the same site and did not change according to the polarity of the S2. These findings indicate that ventricular fibrillation is not an anodally induced phenomenon. The preexisting electrophysiological state at the site of stimulation determines the initiation and maintenance of multiple responses or ventricular fibrillation.

Activity-dependent changes in extracellular potassium and excitability in turtle olfactory nerve

The excitability properties of turtle olfactory nerve (o.n.) were studied in vitro using potassium-sensitive microelectrodes (KSM), a modified sucrose gap chamber, and a standard nerve chamber to measure conduction velocity. A pronounced supernormal period (SNP), as indicated by increased conduction velocity of the o.n. fiber volley, lasting up to several seconds, was observed following a single stimulus. The compound action potential recorded in the sucrose gap chamber showed a prolonged depolarization with a similar time course to the SNP. When stimulation intensity was submaximal the response amplitude, and the extracellular potassium concentration [K+]o, continuously increased during repetitive stimulation. In contrast, when supramaximal stimuli were applied, the amplitude of the o.n. fiber volley was reduced during a high-frequency stimulus train for all responses after the initial one even though latency was maximally reduced, i.e., during supernormal conduction. Superfusion with various levels of K+ elicited changes in the excitability of the o.n. fibers. Small increases in [K+]o above the resting concentration of 2.6 mM led to an increase in resting excitability, whereas larger increases resulted in decreased excitability and conduction block. The SNP was eliminated when extracellular potassium was elevated between 3 and 4 mM above resting levels. Microstimulation of a small bundle of o.n. fibers led to an increase in [K+]o along the bundle but also around adjacent nonactivated fibers. The excitability of these neighboring nonactivated fibers was increased, further indicating the importance of activity-dependent changes in [K+]o in modulating axonal excitability. These results demonstrate the importance of activity-dependent increases in extracellular potassium in modulating nonmyelinated o.n. fiber excitability. They also indicate that increases in [K+]o and an associated membrane depolarization contribute to the increased excitability observed during fiber recruitment and the supernormal period.

Physiological properties of individual cerebral axons studied in vivo for as long as one year

The long-term stability of conduction velocity and recovery processes were studied in a fast-conducting (corticotectal) and in a more slowly conducting (visual callosal) axonal system. Chronic microelectrode recording methods were used in conjunction with antidromic activation via electrical stimulation at one or more axonal site. These methods enabled 54 axons to be studied for greater than 20 days and seven of these cells to be studied for 101-448 days. The conduction velocities of corticotectal axons were characteristic of myelinated axons and were very stable over time. The conduction velocities of most callosal axons were characteristic of nonmyelinated axons, and 68% of callosal axons had conduction velocities that were stable over long periods of time. Of the remaining callosal axons, approximately one third showed an increase in conduction velocity (8-14%), whereas two thirds showed a progressive and systematic decrease in conduction velocity (6-81%). These changes in conduction velocity were distributed along the callosal axon, rather than limited to a single segment of axon. Although the refractory period of callosal and corticotectal axons showed considerable variability over time, the minimal interval between two conducted impulses was stable. The stability of this property was remarkable because the minimal interspike intervals of different axons with similar conduction velocities often differed greatly. Callosal axons show a supernormal period of increased conduction velocity following the relative refractory period and a subsequent subnormal period of decreased conduction velocity following a burst of prior impulses. In different callosal axons the magnitude of the velocity changes (percent change) differs greatly, even among axons of the same conduction velocity. For a given axon, however, these properties are very stable over time. These results on axonal properties may be useful in studies requiring the examination of extracellular responses of individual neurons over long periods of time. Antidromic latency provides a useful means of identifying a cell, particularly when conduction times are long. The stability of the minimal interspike interval and the supernormal period within individual axons make them suitable as ancillary criteria in identifying individual neurons. These three measures are independent of spike amplitude and waveform, and together they provide a "signature" by which individual cortical neurons can be identified over periods that represent a significant portion of the lifespan of adult mammals.

Supernormal conduction in the canine bundle of His and proximal bundle branches

We used close bipolar intramural electrodes and catheter electrodes to study the characteristics of conduction in the bundle of His and proximal bundle branches during premature atrial beats in 17 open-chest anesthetized dogs. The electrophysiological properties of the proximal conducting system were heterogenous. The shortest interval between a normal His bundle response and a premature response that was not accompanied by changes in conduction time (the total recovery time) was 258.8 +/- 23.9 (SD) ms for the proximal His and 310.7 +/- 30.6 ms for the distal His and proximal bundle branches. A period of supernormal conduction, in which the conduction times of premature beats were faster than during earlier or later beats, was localized to the distal portion of the bundle of His and proximal bundle branches. The minimal conduction time during the supernormal period was decreased by 9.6 +/- 4.6% below control diastolic conduction times, and the supernormal period was 61.0 +/- 25.7 ms in duration. The characteristics of the period of supernormal conduction in the distal bundle of His and proximal bundle branches were very similar to those previously found in the peripheral bundle branch-Purkinje system. The mechanism of supernormal conduction in the bundle of His is most probably due to a period of supernormal excitability.