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Biomedical subjects

M N Levy

Publications and source records attributed to M N Levy.

At least 73 records · Page 4Linked to original sources
PubMed1984

The rate of arterial blood pressure change as a factor in the hysteresis of the baroreceptor reflex.

We induced sinusoidal arterial blood pressure oscillations in anaesthetized dogs, and measured the resulting reflex changes in cardiac cycle length. The graphs of cardiac cycle length as a function of systolic arterial pressure displayed considerable hysteresis. The extent of the hysteresis and the direction around the loop varied with the frequency of the pressure oscillations. At relatively low frequencies (0.02 and 0.04 Hz) the loops were predominantly anticlockwise, whereas at higher frequencies (0.08 and 0.16 Hz) the loops were mainly clockwise in direction. In a second group of dogs we stimulated the transected vagus nerves with sequential ramp-like increases and decreases in voltage. The graph of the chronotropic response displayed a prominent anticlockwise hysteresis. Hence the anticlockwise hysteresis which was induced reflexly by cyclic oscillations of systemic arterial pressure is at least partly ascribable to an efferent vagal mechanism.

Animals↗
PubMed1984

Fade of the responses of the isolated, blood-perfused dog atrium to cholinergic interventions.

In the isolated, blood-perfused, canine right atrium, intramural parasympathetic nerve stimulation and intra-arterial infusions of acetylcholine induced substantial negative chronotropic and inotropic responses. The responses to parasympathetic stimulation reached their maximum values quickly, and then usually faded back toward control levels over the next 1 or 2 min of stimulation. The fade of the responses at high stimulation frequencies (greater than or equal to 30 Hz) was significantly greater than that at lower frequencies. The inotropic responses to acetylcholine infusion (1 microgram/min) faded slightly but significantly, whereas the chronotropic responses did not fade at all. These results suggest that the fade of the cardiac responses to parasympathetic stimulation is mainly ascribable to a progressive reduction in the rate of acetylcholine release from the nerve endings, especially at higher stimulation frequencies. The fade of the inotropic responses was more pronounced and had a longer time course than that of the chronotropic responses. Furthermore, the fade of the inotropic responses diminished significantly as the response magnitude was augmented by an increase in stimulation voltage. Conversely, the fade of chronotropic responses was not significantly affected by this intervention. These differences in the inotropic and chronotropic responses to neural stimulation, and the occurrence of a slight fade of the inotropic response to acetylcholine infusion, suggest that in addition to the predominant prejunctional mechanism, a postjunctional phenomenon may also be partly responsible for the fade of the inotropic response to cholinergic interventions.

Acetylcholine↗
PubMed1984

Effects of digoxin on the chronotropic responses to repetitive vagal stimulus bursts in the dog.

We studied the effects of digoxin on the chronotropic responses of the heart to repetitive bursts of vagal stimulation in chloralose-anesthetized dogs. The frequency of the stimulus bursts was increased linearly with time. Over a certain range of frequencies, the cardiac pacemaker became synchronized with the vagal stimulation in a 1:1 ratio of heart beats to stimulus bursts. Digoxin increased the range of cardiac cycle lengths over which 1:1 synchronization occurred during repetitive vagal stimulation. This increment in the range of synchronization varied directly with the dose of digoxin. Before digoxin was given, the range of cardiac cycle lengths over which synchronization occurred when the vagus nerve was stimulated with 10 pulses per burst was 272 +/- 50 (mean +/- SE) ms. However, after a cumulative dose of 120 micrograms/kg-1 digoxin had been given, the range of 1:1 synchronization increased to 396 +/- 32 ms. Digoxin did not appear to have a proportionately greater effect on those processes that take place in the phase of the cardiac cycle during which the pacemaker cells are maximally responsive than on those processes that occur in the phase of the cycle during which the pacemaker cells are minimally responsive. Therefore, we conclude that the augmented entrainment induced by digoxin is ascribable to its tendency to enhance the chronotropic response to vagal stimulation.

Anesthesia↗
PubMed1984

Synchronization of automatic cells in S-A node during vagal stimulation in dogs.

In anesthetized, open-chest dogs, one burst of stimuli was delivered to the left or right vagus nerve each cardiac cycle. The timing of the stimulus bursts relative to the cardiac cycle was varied by a constant, small amount on successive cardiac cycles, until the entire cardiac cycle was scanned. The level of vagal activity was changed by varying the number of stimulus pulses in each burst; two levels of activity were used in each experiment. For a given level of vagal activity, the mean cardiac cycle length and the amplitude of the phase-response curve were significantly greater during right than during left vagal stimulation. These response characteristics increased as the level of vagal activity was augmented. The minimum-to-maximum phase differences of the phase-response curve were less during right than during left vagal stimulation and when the level of vagal activity was increased. The disparities between the minimum-to-maximum phase differences for the right and left vagi are probably ascribable to the associated differences in the overall magnitudes of the chronotropic responses, rather than to any fundamental difference in the innervation of the effector cells by nerve fibers originating from the right and left sides.

Action Potentials↗
PubMed1984

The phase-dependency of the cardiac chronotropic responses to vagal stimulation as a factor in sympathetic-vagal interactions.

We determined the effects of the timing of repetitive bursts of vagal stimulation on the positive chronotropic responses of the heart to trains of cardiac sympathetic nerve stimulation in open-chest anesthetized dogs. Trains of sympathetic stimulation alone, at frequencies of 2 and 4 Hz, decreased the cardiac cycle length by 176 +/- 19 msec (mean +/- SE) and 190 +/- 22 msec, respectively. When bursts of vagal stimuli were given once each cardiac cycle and they were placed at their least effective time in the cycle, sympathetic stimulation at frequencies of 2 and 4 Hz decreased cardiac cycle length by only 107 +/- 8 and 120 +/- 8 msec, respectively. However, when the bursts of vagal stimuli were delivered at their most effective time in each cycle, the same levels of sympathetic stimulation elicited much larger reductions in cardiac cycle length (285 +/- 32 and 330 +/- 32 msec, respectively). Therefore, the effects of sympathetic stimulation were significantly attenuated by the vagal stimuli when the vagal bursts were relatively ineffective. Conversely, the chronotropic effects of the sympathetic stimulation were exaggerated substantially when the vagal stimulus bursts were initially positioned at their most effective time in the cardiac cycle. This latter response is contrary to the characteristic "accentuated antagonism," wherein the effect of any given level of sympathetic stimulation is diminished as the level of vagal activity is increased. This vagally mediated enhancement of the positive chronotropic response to sympathetic stimulation occurs because the phase dependency of the response of the automatic cells to the bursts of vagal stimulation is altered by the increased sympathetic activity.

Animals↗
PubMed1984

Temporal changes in he sympathetic-parasympathetic interactions that occur in the perfused canine atrium.

In the isolated, blood-perfused, canine right atrium, stimulation of the intramural autonomic nerves evoked negative chronotropic and inotropic responses. The responses were not maintained at a constant level during tonic neural stimulation, but they tended to drift back toward their control levels. These time-dependent changes in the cardiac responses were more pronounced the higher the frequency of stimulation. After the beta-adrenergic receptors were blocked in half of the preparations, the negative cardiac responses to autonomic neural stimulation were more pronounced, but the time dependency of those responses was less. After the muscarinic receptors were blocked in the other half of the preparations, only positive responses to neural stimulation were observed. These responses faded significantly at a high stimulation frequency (30 Hz), but not at a lower frequency (5 Hz). The cardiac responses to combined autonomic neural stimulation were substantially more negative than the algebraic sum of the individual responses to sympathetic and parasympathetic stimulation. The extent of this interaction was most pronounced near the beginning of stimulation, but it became less pronounced as the stimulation progressed. Hence, the cardiac sympathetic-parasympathetic interactions change appreciably with time during a continuous train of autonomic neural stimulation.

Animals↗
PubMed1984

Cardiac sympathetic-parasympathetic interactions.

The cardiac response to neural activity in one autonomic division depends on the level of activity in the other autonomic division. The extent of this peripheral interaction varies considerably with the cardiac effector tissue under consideration. In sinoatrial nodal tissue the effect of efferent sympathetic activity is progressively attenuated as the level of vagal activity is increased. A similar type of interaction prevails in the regulation of atrioventricular (AV) junctional pacemaker tissue. Surprisingly, however, an analogous peripheral interaction cannot be detected with regard to the autonomic neural control of AV conduction. Strong vagal activity alone has only a weak negative inotropic effect on the ventricular myocardium. However, in the presence of a substantial background of sympathetic activity, the same level of vagal activity exerts a prominent negative inotropic effect. The peripheral autonomic influence occurs at prejunctional and postjunctional levels. Prejunctionally, acetylcholine (ACh) released from vagal terminals interacts with muscarinic receptors on postganglionic sympathetic terminals to inhibit norepinephrine (NE) release. Postjunctionally, the response of a cardiac effector cell to a given concentration of NE in the biophase will diminish as the concentration of ACh in the biophase is raised.

Animals↗
PubMed1983

Interactions among the critical factors affecting sinus node function: the quantitative effects of the duration and frequency of atrial pacing and of vagal and sympathetic stimulation upon overdrive suppression of the sinus node.

A multifactorial analysis was used in anesthetized dogs in order to characterize the effects of the duration of overdrive, the atrial pacing interval, and the frequencies of vagal and sympathetic stimulation on overdrive suppression of the sinus node. The sinus node recovery time (SNRT) and the summated effect (SE) over the first 20 cardiac cycles were measured with various combinations of the independent variables. We conclude that (1) both the rate and the duration of overdrive have significant effects on SNRT and SE; (2) vagal stimulation has greater effects on SNRT and SE than does the rate or duration of overdrive; (3) sympathetic stimulation had only a small effect on overdrive suppression; and (4) there were significant interactions between vagal stimulation and the duration of overdrive and between the duration and rate of overdrive, but not between sympathetic and vagal stimulation.

Animals↗
PubMed1983

Interactions among heart rate, autonomic activity, and arterial pressure upon the multiple repetitive extrasystole threshold in the dog.

The effects of heart rate, autonomic stimulation, and arterial blood pressure upon the multiple repetitive extrasystole threshold (MRET) were studied after coronary occlusion in anesthetized dogs. The MRET was unaffected by changes in heart rate. Sympathetic stimulation alone reduced the MRET from 52.4 +/- 3.7 (mean +/- SEM) to 41.3 +/- 2.7 mA. Vagal stimulation alone was without effect. During simultaneous sympathetic and vagal stimulation the threshold was 48.7 +/- 3.0 mA. This supports the contention that vagal activity serves mainly to oppose the tendency for sympathetic activity to lower the MRET. Reduction of blood pressure significantly decreased the average MRET from 38.6 +/- 2.5 to 34.4 +/- 1.8 mA. The presence of a post junctional site for the observed sympathetic-vagal interaction was investigated using isoproterenol infusion and vagal stimulation. Infusion of isoproterenol lowered the MRET. Vagal stimulation in this situation raised the MRET; the effect varied directly with the rate of isoproterenol infusion. This suggests that part of the vagal effect is exerted postjunctionally; that is, directly upon the myocardial cell and not merely by inhibition of adrenergic transmitter release at sympathetic nerve endings.

Adrenergic Fibers↗
PubMed1983

Effects of digoxin on the control of heart rate and atrioventricular conduction in the dog.

The effects of digoxin on the chronotropic and dromotropic responses of the heart to autonomic neural stimulation were determined in anaesthetised, open chest dogs. Digoxin did not alter the negative chronotropic response of the heart to vagal stimulation. In contrast, digoxin reduced the positive chronotropic response to sympathetic stimulation by 40%. There was a pronounced vagal-sympathetic interaction such that the positive chronotropic response to strong sympathetic stimulation was attenuated by 72% when a near maximal vagal stimulation was delivered concurrently. However, digoxin did not alter this autonomic interaction. In addition, digoxin did not alter the positive dromotropic response evoked by the sympathetic stimulation. In contrast, digoxin potentiated the increase in A-V conduction time evoked by vagal stimulation (10 Hz) by 147%. No significant vagal-sympathetic interaction in the autonomic control of the dromotropic response was observed; ie, the responses of A-V conduction to combined sympathetic and vagal stimulation were essentially the algebraic sum of the responses to the individual stimulations. This lack of autonomic interaction in modulating A-V conduction time was not altered by digoxin, despite its potentiation of the dromotropic response to vagal stimulation.

Animals↗
PubMed1983

Autonomic nervous control of heart rate: sympathetic-parasympathetic interactions and age related differences.

A factorial experimental design was used to quantify the changes in heart rate produced by stimulation of the cardiac sympathetic and vagal nerves in eleven adult dogs and four puppies, and to quantify the extent of the peripheral sympathetic-vagal interactions. The chronotropic responses to autonomic stimulation were significantly less in the puppies than in the adult dogs, which suggests that autonomic regulation is functionally incomplete in the puppies. In both adult dogs and puppies, the chronotropic responses to autonomic nerve stimulation were bilaterally asymmetrical. The heart rate responses to a given level of right-sided stimulation of either the sympathetic or vagal nerves were greater than those to comparable left-sided stimulation. In both adult dogs and puppies, there were significant sympathetic-vagal interactions, such that the sympathetic enhancement of heart rate was less effective the higher the background level of vagal activity. The sympathetic-vagal interactions were prominent in the puppies as well as in the adult animals, regardless of whether the stimulated sympathetic and vagal nerves were located ipsilaterally or contralaterally to one another. Thus, the mechanisms responsible for the sympathetic-vagal interactions appear to be fully developed in puppies. Also, the cardiac sympathetic nerve endings that originate from one side of the body must lie in close apposition to the cardiac vagal nerve endings that originate from either the same side or from the opposite side of the body.

Aging↗
PubMed1983

Heart rate as a determinant of the decay rate of the cardiac inotropic response to sympathetic nervous activity.

The cardiac responses to sympathetic nerve stimulation were measured in a series of open-chest, anesthetized dogs. In half the animals, the hearts were in a sinus rhythm; in the remaining animals, the hearts were in an atrioventricular (AV) junctional rhythm. Cocaine markedly prolonged the decay times of the chronotropic responses after cessation of sympathetic stimulation, regardless of the type of rhythm. The decay times of the inotropic responses were only slightly prolonged by cocaine in animals with a sinus rhythm, but the prolongations were pronounced in animals with an AV junctional rhythm. The lower basal heart rate appeared to be more responsible for the greater decay times of the inotropic responses in the animals with an AV junctional rhythm than in those with a sinus rhythm. In a second series of dogs, complete heart block was produced, cocaine was given, AND the hearts were paced at four different frequencies. The mean decay time of the inotropic response to sympathetic stimulation varied inversely AND substantially with the pacing frequency. The change in contraction frequency probably affects the rate of neurotransmitter dissipation from the ventricular myocardium, by altering either the coronary blood flow or the massaging action of the cardiac contractions.

Animals↗
PubMed1983

Phasic effects of repetitive vagal stimulation on atrial contraction.

The vagus nerves of anesthetized dogs were stimulated once each cardiac cycle with a brief burst of pulses, and the timing of the stimulus bursts was changed by a fixed increment on successive cardiac cycles. The effects of such vagal stimulation on atrial contraction depended on the number of pulses per stimulus burst, on the interval between pulses within the burst, and on the timing of the stimulus bursts within the cardiac cycle. The vagal stimulus bursts had the least negative inotropic effect when they were given less than 100 msec before the next atrial depolarization, and they were most effective when given about 330 msec before the next atrial depolarization. This dependence of the inotropic response on the timing of the vagal activity within the cardiac cycle indicates that the following conditions must prevail with respect to the vagal innervation of the atrium: (1) the acetylcholine released from the vagal nerve endings is hydrolyzed at a critically rapid rate in the atrial tissues, (2) the neurally released acetylcholine must exert its major influence on atrial contraction during some preferential fraction of the cardiac cycle (presumably, during depolarization), and (3) after a vagal stimulus of a given strength, the concentration of acetylcholine in the region of the myocardial cells will attain its maximum value during this critical phase of the cardiac cycle when the vagal stimuli are given at the optimal time in the cardiac cycle.

Acetylcholine↗
PubMed1983

Neural control of heart rate: a comparison between puppies and adult animals.

The heart rate responses to stimulation of the right and left cardiac autonomic nerves were evaluated in 20 puppies and 17 adult dogs. In every puppy and adult dog, the changes in heart rate were much greater with right- than with left-sided stimulation of the vagal or sympathetic nerves. At maximal stimulation frequencies, the % changes in heart rate (mean +/- S.E.M.) were: right stellate, adults +50.0 (+/- 5.1) and puppies +23.6 (+/- 2.8); left stellate, adults +20.0 (+/- 2.4) and puppies +5.6 (+/- 2.3); right vagus, adults -74.0 (+/- 5.2) and puppies -43.6 (+/- 3.3); and left vagus, adults -44.1 (+/- 2.0) and puppies -24.9 (+/- 2.3). At any given stimulation frequency, the heart rate responses were significantly greater in adult dogs than in puppies, with either stellate or vagal stimulation. In 47% of the puppies and in 11% of the adult dogs, left stellate stimulation had no detectable effect on heart rate, although there was evidence of an increase in blood pressure in each of these animals. In these animals, fibers from the left stellate ganglion did not innervate the sinoatrial node.

Age Factors↗
PubMed1982

Effects of glucagon on cardiac chronotropic response to vagal stimulation in the dog.

Glucagon accelerates the heart independent of sympathetic nervous system stimulation. The effect of glucagon on the chronotropic responses to repetitive bursts of vagal stimulation was determined in open-chest anesthesized dogs. When the cervical vagi were stimulated at constant frequencies, the change in heart rate was not affected by glucagon administration, i.e., no vagolytic effect caused by glucagon was apparent. Thus glucagon did not alter the reaction of acetylcholine with cardiac postsynaptic receptors. When the vagi were stimulated intermittently with one short burst of vagal stimuli delivered each cardiac cycle, the resultant heart period was dependent on the time of vagal stimulus delivery. Both maximum and minimum cardiac cycle lengths obtained during phasic vagal stimulation were decreased by glucagon. As it has been previously demonstrated that vagal impulses to the heart tend to be clustered during certain times of the cardiac cycle, by accelerating the heart glucagon may shift the cardiac response to vagal stimulation.

Animals↗
PubMed1982

Fade of cardiac responses during tonic vagal stimulation.

We applied trains of stimuli to the vagosympathetic trunks of anesthetized dogs and studied the time courses of the resultant chronotropic and inotropic responses. These responses were maximum soon after the onset of the test stimulus train but then declined over the next 1-5 min despite continued stimulation. The fade ratio was defined as the magnitude of this decline divided by the magnitude of the maximum response. For both inotropic and chronotropic responses, maximum increased with stimulation frequency, but the fade ratio did not change. In some experiments, conditioning stimulus trains of variable duration were applied before a standard rest period, after which the test stimulus train was applied. The longer the conditioning period, the lower was the subsequent fade ratio of the inotropic responses to the test stimulation train. In other experiments, a conditioning train of 2 min was applied, and then variable rest periods were interposed before the test train was applied. The longer the rest period, the greater were the subsequent maximum and fade ratios of the inotropic responses to the test stimulus train. These results indicate that some factor persists well after the cardiac responses to a given stimulus, and this factor affects the next response to an identical vagal stimulation. The chronotropic responses faded about three times faster than the inotropic responses. Thus different mechanisms may account for the fade of the inotropic and chronotropic responses.

Animals↗