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PubMed1986

Phasic effects of postganglionic vagal stimulation on atrioventricular nodal conduction.

The effects of postganglionic vagal stimulation (PGVS) on atrioventricular nodal conduction were studied in 15 rabbit atrial-atrioventricular nodal preparations. PGVS was introduced, and sinus cycle length was scanned as independent bursts of subthreshold stimuli were produced in the sinus node and atrioventricular node (AVN). Changes in conduction of atrial impulses to the bundle of His were studied under the following experimental conditions: changes in sinus cycle length resulting from vagal influence on the sinus node, direct vagal stimulation exclusively to the AVN, and during both simultaneous or nonsimultaneous vagal stimulation to sinus node and AVN. The results of the present study showed that the direct effect of PGVS on AVN conduction time at a constant sinus cycle length is phase dependent with maximal prolongation achieved in the first or second beat after introduction of the burst. The interval between the onset of PGVS producing maximal prolongation of conduction time and the following atrial beat was designated the "optimal effective phase." It was shown that the optimal effective phase was a constant parameter for a given preparation and in the present experiments was 321 +/- 16 ms. However, when PGVS was introduced in combination to both nodes while scanning the cycle length, AVN conduction was variable, reflecting both the direct effects of PGVS on the AVN as well as the indirect effects resulting from changes in the sinus cycle length. Notably, it was found that simultaneous PGVS to both the sinus node and AVN usually diminished, whereas appropriate nonsimultaneous PGVS accentuated the typical phasic dependency of AVN conduction time. Additionally, vagally induced prolongation of the sinus cycle length was found to be accompanied by changes in the time of depolarization of the inputs to the AVN, thus influencing AVN conduction and facilitating reentry. These interactions between changes in the sinus cycle length and concomitant changes in the effectiveness of vagal influence on the AVN can be used to explain complexities of AVN conduction during increased vagal activity.

Animals↗
PubMed1986

Vagally induced hyperpolarization in atrioventricular node.

The effects of postganglionic vagal stimulation on atrioventricular nodal conduction were studied in 12 rabbit atrial-atrioventricular nodal preparations. Vagal stimulation was introduced in the sinus and atrioventricular nodes, separately or in combination, using single bursts of subthreshold stimuli. The sinus cycle length was scanned to identify the phasic effect of vagal stimulation. Action potentials from cells in the AN, N, and NH regions of the atrioventricular node were recorded by microelectrode techniques. Vagally induced hyperpolarization of cells in the atrioventricular node resulted in a phase-dependent prolongation of conduction time and reflected the level of residual hyperpolarization at the moment of arrival of the next atrial beat at the atrioventricular nodal input region. Vagally induced hyperpolarization was membrane potential dependent, although its overall time course was similar at different phases. Increased diastolic depolarization followed the maximal hyperpolarization. This "rebound" observed at certain phases was responsible for paradoxical shortening of the conduction time after vagal stimulation. The predominant effects of local vagal stimulation in the atrioventricular node were observed in cells in or near the N region. Slower rate of rise, shorter amplitude and duration, as well as step formations were among the changes in action potentials recorded from these cells. The effects of vagal stimulation were inhomogeneous between different regions of the atrioventricular node as well as within the N region, producing alternative pathways of conduction and the potential for reentry. The concomitant changes in sinus cycle length resulting from vagal stimulation in the sinus node region altered the phasic effects of vagal stimulation introduced in the atrioventricular node. This was related to a direct influence of the prolonged sinus cycle length on atrioventricular nodal refractoriness as well as an indirect effect on the degree of residual vagally induced hyperpolarization at the moment of arrival of the delayed atrial beat. These findings provide mechanistic explanations for the complex effects of vagal stimulation on atrioventricular nodal conduction.

Animals↗
PubMed1989

Brief vagal stimuli and AV conduction in dogs: effects on retrograde exceed antegrade.

We opened the chests of 20 mongrel dogs (16-28 kg) that were anesthetized with pentobarbital sodium (22 mg/kg), given propranolol (1 mg/kg), and bipolar catheters placed into the right atrium and ventricle. We crushed the sinoatrial (SA) node and paced the heart to produce either an antegrade (A-V) or a retrograde (V-A) conduction (where A is atrial activation and V is ventricular activation). Both cervical vagosympathetic trunks were ligated and connected to electrodes that were driven by a computer-controlled, isolated stimulators. Three brief vagal stimulus bursts (at the same intensity but at different times in the cardiac cycle) were given at least 1 min apart, the pacing site was changed, and the identical three-stimulus bursts were again applied. This procedure was continued until the phase of the stimulus had scanned the entire cardiac cycle. Forty-four sets of vagal effect curves were generated. The composite data indicate that brief vagal stimuli have about twice the effect on the peak amplitude of the change in retrograde than in antegrade AV nodal conduction in the dog. Unexpectedly, the duration of the parasympathetic effect is also considerably greater (approximately 40%) and the decay is slower (approximately 48%) for retrograde than for antegrade conduction, even when the vagal effect curves have been normalized to the same amplitude. This latter result suggests that some factor other than diffusion and inactivation of ACh determines the duration of the A-V conduction response to a brief vagal stimulus.

Animals↗
PubMed1985

Calcium-dependent potassium conductance in rat supraoptic nucleus neurosecretory neurons.

Intracellular recordings of rat supraoptic nucleus neurons were obtained from perfused hypothalamic explants. Individual action potentials were followed by hyperpolarizing afterpotentials (HAPs) having a mean amplitude of -7.4 +/- 0.8 mV (SD). The decay of the HAP was approximated by a single exponential function having a mean time constant of 17.5 +/- 6.1 ms. This considerably exceeded the cell time constant of the same neurons (9.5 +/- 0.8 ms), thus indicating that the ionic conductance underlying the HAP persisted briefly after each spike. The HAP had a reversal potential of -85 mV and was unaffected by intracellular Cl- ionophoresis of during exposure to elevated extracellular concentrations of Mg2+. In contrast, the peak amplitude of the HAP was proportional to the extracellular Ca2+ concentration and could be reversibly eliminated by replacing Ca2+ with Co2+, Mn2+, or EGTA in the perfusion fluid. During depolarizing current pulses, evoked action potential trains demonstrated a progressive increase in interspike intervals associated with a potentiation of successive HAPs. This spike frequency adaptation was reversibly abolished by replacing Ca2+ with Co2+, Mn2+, or EGTA. Bursts of action potentials were followed by a more prolonged afterhyperpolarization (AHP) whose magnitude was proportional to the number of impulses elicited (greater than 20 Hz) during a burst. Current injection revealed that the AHP was associated with a 20-60% decrease in input resistance and showed little voltage dependence in the range of -70 to -120 mV. The reversal potential of the AHP shifted with the extracellular concentration of K+ [( K+]o) with a mean slope of -50 mV/log[K+]o.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1976

Dissociation and delayed conduction in the canine right bundle branch.

Bipolar electrograms were recorded from five to six sites on the septal right bundle branch (RBB) using a multielectrode patch in ten mongrel dogs. Antegrade activation was recorded along the right bundle during sinus rhythm and during right atrial pacing at varying heart rates. Retrograde activation was produced by pacing from right ventricular epicardium. Right bundle conduction velocities varied from 1.4 to 3.3 m/sec (mean 2.0 m/sec) for antegrade conduction and from 1.8 to 2.7 m/sec (mean 2.1 m/sec) for retrograde activation. Varying degrees of conduction delay were elicited by premature stimulation and mechanical pressure to the right bundle. The conduction delays occurred over small segments of the right bundle branch with regeneration of normal propagation velocity distal to the region of block. The conduction delays were associated with fragmentation of the RBB electograms with initiation of delayed activation waves which traveled variable distances antegrade and retrograde. These data show that stress-induced longitudinal dissociation may produce delayed activation waves within the right bundle branch which may simulate re-entrant arrhythmias.

Animals↗
PubMed1986

The effects of procainamide on conduction in anisotropic canine ventricular myocardium.

Although conduction velocity in cardiac tissue is dependent on fiber orientation, the influence of commonly used antiarrhythmic agents on conduction longitudinal and transverse to such fibers is unknown. We evaluated the effects of procainamide on conduction velocity and intracellular potentials in vitro during conduction longitudinal and transverse to fiber orientation in epicardial strips obtained from areas of uniform fiber orientation from 15 adult mongrel dogs. Ventricular epicardial strips demonstrated marked anisotropy. At a pacing cycle length of 1000 msec, mean conduction velocity longitudinal to fiber orientation averaged 0.602 +/- 0.051 m/sec and mean conduction velocity transverse to fiber orientation was 0.186 +/- 0.024 m/sec, resulting in a ratio of longitudinal to transverse conduction velocities of (theta L/T) 3.27 +/- 0.38. After the addition of procainamide, conduction velocity decreased to 0.532 +/- 0.062 m/sec longitudinal to fiber orientation and to 0.174 +/- 0.023 m/sec transverse to fiber orientation resulting in a decrease of theta L/T to 3.09 +/- 0.37 (p less than .05 vs control). Before the addition of procainamide, when pacing at progressively shorter cycle lengths, conduction velocity longitudinal to fiber orientation was relatively unchanged, whereas conduction velocity transverse to fiber orientation decreased resulting in an increase in theta L/T. After the addition of procainamide, conduction velocity at shorter pacing cycle lengths decreased both longitudinal and transverse to fiber orientation demonstrating the well-known use-dependent effect of procainamide. However, in contrast to control conditions, conduction velocity longitudinal to fiber orientation was slowed by a greater extent than the conduction transverse to fiber orientation, resulting in an even greater decrease in theta L/T. To investigate the effect of differences in drug binding during propagation in different directions, we examined conduction velocity during alternations in pacing direction and compared it with velocity during steady-state pacing. At a pacing cycle length of 1000 msec, no difference was observed between the initial conduction velocity after changing pacing directions and the steady-state conduction velocity. At pacing cycle lengths shorter than 1000 msec, when changing from transverse to longitudinal conduction, there was an initial drop in normalized conduction velocity that was present on the first beat of longitudinal conduction; however, with continued pacing in a longitudinal direction there was a further decrease in conduction velocity.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1983

Alterations in electrophysiological properties during canine myocardial ischemia--variation with location in the ischemic zone in vivo.

We examined electrophysiological properties of the ischemic myocardium of the canine heart. Multiple bipolar electrodes for stimulation or for recording electrograms were placed on the epicardial surface and at the endocardium of the ventricle. The time course of changes in excitability threshold, in effective refractory period and in local conduction time during ischemia was estimated at the epicardial and endocardial sides of the central ischemic zone, at the epicardial side of the peripheral ischemic zone and at both sides of the normal zone. Soon after left anterior descending coronary artery occlusion, a rise of excitability threshold, a lengthening of effective refractory period and a prolongation of conduction time consistently occurred in all portions of the ischemic zone. The degree of changes, however, was not uniform: it was greater at the epicardial side of the central ischemic zone. In most experiments, the changes reached maximum within 10 min after occlusion. Then, altered electrophysiological properties recovered to some extent or stabilized. The results indicate that electrophysiological properties deteriorate momentarily after coronary occlusion but then recover or stabilize, and that their changes during acute ischemia are not uniform in the ischemic region but severer at the central zone and epicardial side.

Animals↗