Slow Rate Of Rise Research Articles

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.

Fatigue of voluntary contractions in normal and myasthenic human subjects.

The effect of fatigue developed during 96 repeated rapid maximal voluntary finger muscle contractions (MVC), 12 contractions per minute, was followed in 4 control subjects and 4 myasthenic patients. The tension-time integral (T-TI) was determined during either the first 1 or 1.25 s of each contraction. Fatigue decreased the T-TI by 21% in the control subjects and by 65% in the patients. While ordinary MVC showed a slow rate of rise of tension and gradually increasing electromyographic activity, rapid MVC from both groups showed a steep rate of rise of tension, a 'notch' after about 0.3-0.4 s separating two relative maxima and a larger electromyographic activity during the first half second of the contraction. The mechanograms from rapid MVC were divided by an arbitrary straight line connecting the starting pint of the contraction curve and the notch. The line separated an area (N X s) above and to the left (alpha-component) from an area below and to the right (beta-component of the line. Fatigue affected the beta-component selectively in both control subjects and myasthenic patients. Only when the beta-component was reduced by more than 80%, was a reduction of the alpha-component also seen. At any time during a sustained contraction, the patients could briefly increase their instantaneous strength, but for only about one half second. The results suggest that human muscle contractions can be divided into two parts with a different sensitivity to fatigue in both control subjects and myasthenic patients.

Generation of an unusual depolarizing response in rabbit primary afferent neurones in the absence of divalent cations.

The effects of divalent cations on responses to 5-hydroxytryptamine (5-HT), gamma-aminobutyric acid (GABA) and 1,1-dimethyl-4-phenyl piperazinium (DMPP) were investigated using a sucrose-gap method to record population responses. In Ca-free medium responses to 5-HT were enhanced, those to DMPP depressed and those to GABA unchanged. In Mg-free medium responses to 5-HT were unchanged, while those to DMPP and GABA were depressed. Removal of both Ca and Mg from the superfusion medium caused a small reduction of GABA responses and a large reduction of DMPP responses. Responses to 5-HT were not only greatly potentiated but were changed in character; the depolarizing phase became sigmoid and the dose dependence between quantity of 5-HT and response magnitude was lost as if 5-HT were triggering an all-or-nothing phenomenon. Dose--response relationships for GABA were normal in the large majority of preparations. In about 10% of preparations, supramaximal amounts of GABA or DMPP evoked large responses of a similar character to those evoked by 5-HT. The large responses, generated by an unknown mechanism, were termed X responses. Further reduction in tissue divalent cations by EGTA (1 mM) caused X responses to be generated spontaneously. Ca, Mg, Mn or Co (1 mM) could suppress X responses. DMPP responses, reduced in Ca/Mg-free medium, were largely restored by 1 mM-Ca. Depression of GABA responses in Ca/Mg-free medium could be entirely attributed to the absence of Mg, Mn being able to substitute for Mg. X responses were generated only after equilibration for 1 h with Ca/Mg-free medium. Attempts to manipulate [Ca]i with dinitrophenol or caffeine did not produce the conditions under which X responses were generated. Intracellular records of responses to 5-HT, GABA or DMPP showed that cells with A fibres responded to GABA but not to 5-HT or DMPP. Fifty-four out of sixty-seven cells with C fibre axons (80%) were depolarized by 5-HT, thirty-seven out of forty-nine (76%) by DMPP and forty out of fifty-seven (70%) by GABA. Eighteen out of thirty-eight (47%) C cells were depolarized by all three agents. Some C cells were very sensitive to 5-HT, 10(-6) M evoking a substantial response. In most, responses to 10(-5) M-5-HT had a slower rate of rise than responses to 10(-4) or 10(-3) M-GABA or DMPP, yet lower 5-HT concentrations normally elicited X responses in sucrose-gap experiments whereas GABA or DMPP normally did not.(ABSTRACT TRUNCATED AT 400 WORDS)

A new approach for determining permeability characteristics of rock using slug testing techniques

A new technique of determining hydraulic flow characteristics of rock in the laboratory is presented. The technique is a laboratory simulation of a well known in situ ‘slug’ testing method where aquifer parameters are determined by the removal of water slug in a test borehole. The time taken for the water level in the borehole to return to its original rest level, is observed. The results are treated using an analytical technique, first developed by Theis [1]. The laboratory technique involves a test on a very small scale, with a slow rate of rise of water in a drill hole. The laboratory equipment and test procedure are described together with the advantages and limitations of the system. The technique offers an inexpensive, simple and effective method for determining the permeability of standard core samples, whilst keeping the amount of sample preparation to a minimum. The technique offers a potential for testing of most rock types under a variety of loading conditions.

Estimation of myocardial infarct size by digital computer analysis of the VCG

This study described the linear relationship of the myocardial infarct size, measured postmortem, to the integral of the sequential vector spatial magnitudes analyzed at 400 samples per second during the initial period of abnormal depolarization (IAD) in 25 patients with myocardial infarction (MI) and ten controls. The equation for the fitted regression line was: %MI = -0.35 + 3.33 IAD; r = .90; p less than .001. The duration of abnormal depolarization was determined by two computer algorithms: first, using the classical method of pathological Q wave duration, whenever possible; and a new method of measurement of an abnormally slow rate of rise of vector spatial magnitude with time (dm/dt), when there were no Q waves in the Frank orthogonal lead input signals. There was not a significant difference in the mean values of IAD of the MI group or the control group calculated by the two algorithms.

Electrical properties of cultured heart cell reaggregates from newborn rat ventricles: Comparison with intact non-cultured ventricles

The electrophysiological properties of cultured rat heart cells were investigated and compared with those of cells in intact hearts of the same age rats. Reaggregates (100 to 200 μm diameter) from newborn rat hearts (ventricles) were prepared from collagenase-hyaluronidase-dissociated cells and cultured for periods up to 7 days. Intracellular micro-electrode recordings were made using standard techniques. Ventricular reaggregates cultured under standard conditions had a low resting potential (−67 ± 1.5 mV) and the action potentials had a slow rate of rise (18 ± 1.4 V/s). Tetrodotoxin (5 × 10 −6 m) decreased only slightly the rate of rise and verapamil (10 −6 m) inhibited completely the action potentials. In contrast the ventricular action potentials recorded from isolated ventricles were characterized by a high resting potential (−77 ± 0.7 mV) and a fast rate of rise (80 to 193 V/s). Tetrodotoxin (5 × 10 −6 m) decreased the rate of rise and verapamil (10 −6 m) only depressed the plateau level of the action potentials. In cultured reaggregates hyperpolarizing current pulses increased the rate of rise. This effect was prevented by tetrodotoxin. Reducing the amount of fibroblasts in the reaggregates by using the differential attachment technique, caused the AP parameters to become similar to those found in non-cultured cells. We conclude that, under certain conditions (e.g. removal of fibroblasts) fully differentiated properties can be maintained in reaggregate cell cultures. Thus, as in the case of cultured chick heart cells, cultured rat heart cells can be maintained in vitro in a highly differentiated state.

Verapamil

The advent of intracellular microelectrode recordings has led to an understanding of the ionic changes and mechanisms involved in the cardiac action potential and in cardiac pacemaker function. Direct recordings from the sinus node have led to insight into mechanism of the sinus-node automaticity. An inward (depolarizing) current carried by calcium and sodium ions termed the "slow channel" is believed to play a major role in impulse formation within the sinus node.¹The slow channel is characterized by a slow rate of rise (low change in voltage per unit of change in time) and initiation at lower, less negative levels of membrane potential than the normal fast sodium spike. In addition to the sinus node, the atrioventricular (AV) junction appears to be largely dependent on the slow response for impulse formation and conduction. The slow channel has also been implicated in the genesis of arrhythmias. As it is activated

Verapamil. A new class of antiarrhythmic agents with a variety of beneficial cardiovascular effects

The advent of intracellular microelectrode recordings has led to an understanding of the ionic changes and mechanisms involved in the cardiac action potential and in cardiac pacemaker function. Direct recordings from the sinus node have led to insight into mechanism of the sinus-node automaticity. An inward (depolarizing) current carried by calcium and sodium ions termed the is believed to play a major role in impulse formation within the sinus node.1The slow channel is characterized by a slow rate of rise (low change in voltage per unit of change in time) and initiation at lower, less negative levels of membrane potential than the normal fast sodium spike. In addition to the sinus node, the atrioventricular (AV) junction appears to be largely dependent on the slow response for impulse formation and conduction. The slow channel has also been implicated in the genesis of arrhythmias. As it is activated

Electrophysiological recordings from spontaneously contracting reaggregates of cultured smooth muscle cells from guinea pig vas deferens.

Smooth muscle cells were enzymatically dispersed from vasa deferentia of adult male guinea pigs (250-400 g). These cells reassociated in vitro to form monolayers and small spherical reaggregates (0.05-0.3 mm in Diam). Within 48 h of being placed in culture, cells in both types of preparation began to contract spontaneously. The contractions were rhythmic and slow. Cells in the monolayers stopped contracting after approximately 1 wk in vitro, but the reaggregates continued to contract spontaneously for at least 3 wk. Electron microscopy of the reaggregates revealed the presence of thick and thin myofilaments. Overshooting action potentials were recorded in many of the cells penetrated (primarily in reaggregates), and were accompanied by visible contractions of the aggregate or monolayer. Quiescent cells could often be excited by intracellularly applied depolarizing and hyperpolarizing (anodal-break) current pulses. The resting potentials had a mean value of -58 +/- 2 mV. The action potentials were usually preceded by a spontaneous depolarization. The action potentials had slow rates of rise (1--4 V/s) which were unaffected by tetrodotoxin (TTX, 1 microgram/ml), a known blocker of fast Na+ -channels. Verapamil (1 microgram/ml) blocked the action potentials. The mean value of input resistance was 6.9 +/- 0.5 M omega (n = 12). These electrophysiological properties are similar to those of intact adult vas deferens smooth muscle cells. Thus, the cultured adult vas deferens smooth muscle cells retain their functional properties in vitro even after long periods.

BRAIN EXTRACELLULAR POTASSIUM AND ENERGY METABOLISM DURING ISCHEMIA IN JUVENILE RATS AFTER EXPOSURE TO HYPOXIA FOR 24 h

Abstract— The ischemia‐induced change of brain extracellular potassium concentration [K+]e and brain energy metabolism was studied following decapitation of normal 7‐dav‐old rats and 7‐day‐old rats exposed to a simulated altitude of 6000 m (pO2= 70 mm Hg) for 24 h. Initially there was in both groups a slow rate of rise of [K +]e followed by a faster rise until a steep increase occurred. In the group exposed to hypoxia the initial rate of rise was lower and the duration until the steep increase twice as long as in the normal group. Energy consumption expressed as Δ#P and the rates of lactate accumulation were similar in the two groups in the first minute following decapitation. After 2 min the Δ#P and the rate of lactate accumulation was higher in the group exposed to hypoxia. These findings are explained by a doubling of the glucose concentration in the brain of the rats exposed to hypoxia, permitting anaerobic glycolysis to maintain ATP regeneration for a longer time during ischemia.

The extracellular potassium concentration in brain cortex following ischemia in hypo- and hyperglycemic rats.

The extracellular potassium concentration, [K+]e, was measured in the brain cortex of hypo-, normo- and hyperglycemic rats following brain ischemia. The increase in [K+]e in control rats could be characterized by 3 phases: an initial slow rate of rise where the [K+]e rose in 2 min from 3 to 9 mM followed by an abrupt, steep increase to 60 mM within 10 s and finally a slow rise to 80 mM. In the hyper- and hypoglycemic rats the same pattern appeared, but there were significant differences in the time course. The duration of the initial phase was approximately doubled in the hyperglycemic and halved in the hypoglycemic group. The [K+]e at which the steep increase was elicited was 8--10 mM in all groups. It is concluded that the duration of the initial phase is dependent upon available stores of glucose in the brain.

Significance of 2,4‐dinitrophenol action on spinal motoneurones.

1. Extracellular iontophoretic applications of DNP lead to an increase in the membrane conductance of cat spinal motoneurones, manifested by a rise in input conductance, a slower rate of rise and fall of action potentials, and occlusion of the afterhyperpolarization. 2. There is also some hyperpolarization, but the reversal potential for the action of DNP is only about 12 mV more negative than the resting potential. 3. These effect of DNP can be abolished or significantly reduced by intracellular injections of EGTA. On the other hand, DNP can partly reverse the decreased conductance and the depression of the slow afterhyperpolarization caused by EGTA. 4. Intracellular injections of DNP also induce a rise in input conductance; when repeated, they tend to have a depolarizing effect, mainly irreversible. 5. It is concluded that DNP acts principally inside the motoneurone, by liberating bound internal Ca, the free Ca ions then raising membrane conductance, especially GK.

EPSPs of masseter motoneurons evoked by stimulation of low-threshold infraorbital nerve afferents in cat

Stimulation of the infraorbital nerve at strengths 1.4–2.5 times higer than the threshold of excitation of A fibers in cats anesthetized with chloralose and pentobarbital evoked EPSPs with an amplitude up to 3.0 mV and a duration of 9–15 msec in 69% of masseter motoneurons after 1.5–3.0 msec. These EPSPs were complex and formed by summation of simpler short-latency and long-latency EPSPs. The short-latency EPSPs appeared in response to infraorbital nerve stimulation at 1.1–1.5 thresholds and had a slow rate of rise (2.5–4.5 msec, mean 3.7±0.4 msec), low amplitude (under 2.0 mV), and short duration (5–6 msec). Their latent period varied from 1.5 to 3.0 msec (mean 2.1±0.2 msec). The shortness of the latent period and its constancy during stimulation of the nerve at increasing strength, and also the character of development of facilitation and inhibition of the EPSP during high-frequency stimulation suggests that these EPSPs are monosynaptic. The slow rate of rise suggested that these EPSPs arise on distal dendrites of the motoneurons. Long-latency EPSPs appeared 7–9 msec after stimulation of the infraorbital nerve at 1.1–1.5 thresholds. Their amplitude reached 1.5–2.0 mV and their duration 7–9 msec. The long duration of the latent period combined with low ability to reproduce high-frequency stimulation (up to 30/sec) points to the polysynaptic origin of these EPSPs.

Interaction between longitudinal and circular muscle in intestine of cat.

1. Slow waves recorded from isolated longitudinal muscle averaged 13 mV and had slow rate of rise (0.04 V/sec) whereas when recorded from intact segments the amplitude averaged 27 mV and the rate of rise was more rapid (0.09 V/sec), often with a notch between the initial peak and the plateau. Membrane potentials of longitudinal muscle were similar in isolated and intact preparations (- 66 mV). Resting potentials of circular muscle averaged - 67 mV.2. Small bundles of circular muscle tested in the double sucrose gap produced activity, either spontaneously or in response to stimulation, which fell into three categories: fast spikes (50-200 msec duration), slow spikes (1-5 sec duration), and small graded responses. The duration of fast spikes could be increased severalfold by the addition of TEA; the graded responses were converted to full-sized spikes by TEA.3. Treatment of circular muscle with Ca-free Krebs solution eliminated spikes, and in intact preparations reduced the amplitude and rate of rise of slow waves and eliminated the notch on slow waves.4. Current-voltage curves of longitudinal muscle show delayed rectification in the depolarizing quadrant; similar curves of circular muscle show anomalous rectification, i.e. a region where a very small current causes a large voltage change.5. Non-polarized electrotonic coupling between longitudinal and circular layers indicates low-resistance pathways. Apparent space constants of longitudinal muscle are greater when attached to circular muscle than when isolated.6. It is concluded that small slow potentials originate rhythmically in longitudinal muscle, that these spread passively to circular muscle where a regenerative amplification occurs which depends on Ca conductance and the amplified slow waves spread back to the longitudinal layer. In the intact intestine pacemaking is, therefore, separate from propagation and the circular muscle provides the bulk of depolarizing current for propagation.

Extracellular potassium concentration in juvenile and adult rat brain cortex during anoxia.

The extracellular K+ concentration, ([K]e), in the brain cortex of rats at different ages was measured by means of K+-sensitive microelectrodes. [K]e was between 3 and 5 mM at all ages. Following nitrogen inhalation there was an increase in [K]e which exhibited a sigmoid pattern in every age group: Firstly, there was a slow rate of rise which was followed by a sudden, steep increase where the [K]e rose to about 70 mM. During the subsequent 5-10 min a plateau value of about 90 mM was reached. The prominent difference between the age groups was the time until the steep rise began. The time to the steep increase in [K]e and the [K]e at the start of the steep was inversely related to the age of the animal. A close relation was found between the time to the start of the steep increase and the time to the last gasp during nitrogen breathing (r = 0.98). It is suggested that the different resistence to anoxia in young and adult animals is related to differences in the ability to keep near normal potassium gradients across the cells in the brain.

Electrophysiological recordings from spontaneously contracting reaggregates of cultured vascular smooth muscle cells from chick embryos

Single cells were trypsin-dispersed from blood vessels (great vessels near the heart and mesenteric vessels) of 10–20 day chick embryos, and induced to reaggregate into small spheres (0.1–0.5 mm ∅) either by gyration or by plating on cellophane. Many reaggregates contracted spontaneously or in response to electrical stimulation during culture periods of up to 6 weeks. When the spherical reaggregates were allowed to adhere to a glass substrate, cells emigrated from the spheres to form aprons of monolayered cells which continued to contract. Thick and thin myofilaments (mean diameters of 146 and 65 Å, respectively) were observable in a large fraction of cells studied in electron micrographs. Vascular smooth muscle (VSM) cells were identified in the reaggregates by recording resting potentials of −40 to −60 mV, and by action potential generation. The action potentials were preceded by pacemaker potentials, had slow rates of rise (<20 V/sec), and were insensitive to tetrodotoxin (TTX). Although the action potentials depend on an inward slow current, D-600 did not block the action potentials of the VSM cells. Reaggregates of atrial cells, produced at the same time for comparison, had larger resting potentials (up to −80 mV), less automaticity, fast rates of rise (mean of about 85 V/sec), and complete TTX sensitivity, thus indicating dependence on fast Na + channels. These findings indicate that identifiable VSM cells can be successfully maintained in primary culture for several weeks, and these cells retain electrical and contractile properties similar to those of smooth muscle cells in intact adult blood vessels. This preparation provides a convenient system for electrophysiological and pharmacological studies of VSM cells.

Effects of stimulating the acetylcholine receptor on the current-voltage relationships of the smooth muscle membrane studied by voltage clamp of potential recorded by micro-electrode.

1. A double sucrose-gap voltage-clamp technique is described for use on smooth muscle strips longer than about 2 mm. It involves intracellular recording by microelectrode of the membrane potential of a narrow region of the strip ("node") sandwiched between two streams of deionized sucrose solution. Current was passed into the node across one or both sucrose streams. 2. Preliminary experiments in which potential was recorded intracellularly at two points during polarization of a "short cable" preparation, formed by folding over a strip of smooth muscle, suggested that a node width of less than 0-15 mm was needed to achieve uniform potential during inward current flow. However, when node width between sucrose-gaps was reduced to 0-5 mm, spontaneous electrical activity was lost, and below 0-5 mm spike threshold was raised and the regenerative spike became graded. The currents flowing during the application of rectangular voltage-clamp command potentials were described. 3. Using taenia smooth muscle it was shown by recording with a second, independent micro-electrode that potential was not uniform for up to 200 ms or more following a step change in potential under voltage-clamp in nodes 0-4-0-5 mm wide where current was passed across both sucrose gaps. However, reasonably uniform nodal potentials were obtained using ramps with relatively slow rates of rise (25 mV/s). 4. Using such slow ramp commands under voltage clamp, the effects of carbachol on the current-voltage relationship of longitudinal muscle of ileum and taenia were studied in hypertonic solution. 5. In the presence of carbachol (10(-6) to 10(-5) g/ml.) additional inward current flowed across the membrane (in some experiments an equilibrium potential was observed at which this current reversed direction). The magnitude of this additional current was linearly related to potential at potentials negative to the resting potential. At potentials positive to the resting membrane potential, this additional current increased with depolarization over the range -40 to -10 mV; in ileum the effect of this additional inward current on the current-voltage relationship was to produce a region of net inward current where before, in the absence of carbachol, a net outward current existed. In taenia the additional inward current flowing in the presence of carbachol was too small to produce a region of net inward current; thus carbachol produced regenerative slow oscillations of potential (slow waves) in ileum but not in taenia. 6. These results support a previous suggestion that activation of the acetylcholine receptor of ileal smooth muscle produces an additional inward current in the membrane which increases with depolarization and is responsible for the regenerative slow waves seen when muscarinic stimulants are applied. A similar effect apparently operates in taenia but the additional inward current is too small to produce regenerative slow waves.

CORRELATION BETWEEN PLASMA QUINIDINE AND CARDIAC EFFECT

1 The relationship between serum quinidine levels and rate-corrected QT (QTc) interval after administration of single identical doses of quinidine was assessed. Quinidine concentrations were determined by a modification of Hamfelt & Malers' (1963) method. The significance and clinical application of our findings is discussed. 2 Individual responses (both in quinidine concentration and QTc prolongation) were variable, though the variation was no greater with QTc prolongation response than with serum quinidine levels. A significant peak in QTc prolongation occurred after quinidine administration and this was not accompanied by a similar peak in quinidine levels. There was some correlation (r = 0.53) between serum quinidine levels and QTc interval but a better correlation was found between rate of rise of quinidine concentration and QTc prolongation (r = 0.87). 3 One individual showed marked QTc prolongation with slow rate of rise of quinidine levels. Red cell quinidine levels were lower in this individual and he may be showing increased myocardial sensitivity to quinidine.

The locust jump

The locust jumps by a rapid extension of its metathoracic tibiae. The comparatively slow rate of rise of tension of the extensor tibia muscle means that if it is to shorten rapidly, it must develop tension isometrically prior to the jump by co-contracting with the flexor muscle. The extensor muscle is far stronger than the flexor and thus there has to be considerable structural specialisation of the joint to enable the flexor to prevent the tibia moving under the extensor tension. The geometry of the joint gives the flexor muscle a very large mechanical advantage over the extensor in the fully flexed position. This mechanical advantage decreases rapidly as the joint extends so that the residual flexor tension does not slow down the movement (Fig. 4). There is also a locking device associated with the flexor tendon which is engaged when the tibia is fully flexed and which holds it in this position against the developing extensor force (Fig. 5).

Impulse propagation through the cardiac junctional regions of the axolotl and the turtle.

In isolated preparations from the axolotl and turtle hearts thepropagation of impulses through different cardiac tissues was studied. Intracellular records were taken from the various types of fibers. Notchedaction potentials were recorded in two junctional regions: the atrioventricularring (A-V. R.) and the ventricle-bulbus cordis (V-B. C.).The action potential recorded in either the A-V. R. or the V-B. C.regions has a notch in its depolarization phase. The temporal occurrenceof the notch was determined by the activation of the correspondingneighboring tissues. The two components given by the notch can beseparated out by using different experimental variables.The A-V. R. and the V-B. C. junctional regions are constitutedby groups of horizontal fibers. When these are severed from the otheradjacent cardiac tissues, it can be seen that the junctional fibers presentspontaneous activity and that the action potential recorded from themis characterized by a slow rate of rise, absence of a notch, and a slowdiastolic depolarization.In these junctional regions it was found that the conduction velocitywas lower than that of any of the other cardiac tissues (Table 1). Thesejunctional regions are preferential sites for delays and blockages inpropagation.The morphological studies revealed that the cells of the A-V intermediateregion are characterized by:(a) small cross sectional diameter ofcytoplasmic extensions;(b) isolated and scanty myofibrils;(c) abundantglycogen deposits; and (d) sparsity of junctional contacts.The electrophysiological and ultrastructural characteristics reportedhere, point towards the conclusion that in the axolotl and turtle hearts themechanisms that underlie the delays in propagation in the junctional regions are similar to those of the mammalian in spite of the absenceof specialized conductive tissues in the lower species.