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Biomedical subjects

M N Levy

Publications and source records attributed to M N Levy.

At least 91 records · Page 5Linked to original sources
PubMed1982

Effects of autonomic activity and changes in heart rate on atrioventricular conduction.

The effects of autonomic neural stimulation and changes in atrial pacing frequency on atrioventricular (AV) conduction were determined in anesthetized open-chest dogs. Increases in vagal stimulation frequency and in pacing rate significantly increased the AV interval, whereas increases in sympathetic stimulation frequency reduced the AV interval. Vagal stimulation (1.4 Hz) prolonged the AV interval by 17 ms when the atrial pacing rate was 2 Hz. On the other hand, the same vagal stimulation increased the AV interval by 29 ms when the pacing rate was 2.73 Hz. In addition, sympathetic stimulation (1.2 Hz) reduced the AV interval by 29 ms when the pacing rate was 2 Hz. In contrast, the same sympathetic stimulation reduced the AV interval 54 ms when the pacing rate was 2.73 Hz. However, the increase in vagal stimulation did not significantly alter the positive dromotropic response of the AV node to sympathetic stimulation. Therefore, the response of AV conduction to combined sympathetic and vagal stimulation was essentially the algebraic sum of the responses to the individual stimulations. Furthermore, the level of activity in one autonomic division did not alter appreciably the interaction between the pacing rate and the activity in the other autonomic division; i.e., the interaction between pacing rate, sympathetic stimulation, and vagal stimulation was not significant.

Animals↗
PubMed1981

Changes in vagal phasic chronotropic responses with sympathetic stimulation in the dog.

Sympathetic stimulation both shortens the cardiac cycle and potentiates the cardiac response to vagal stimulation. In the present study the effects of sympathetic stimulation on the chronotropic responses of the heart to brief bursts of vagal stimulation were determined in open-chest anesthetized dogs. The sinoatrial nodal pacemaker cells demonstrate a paradoxical response to repetitive bursts of vagal stimuli over a certain portion of the cardiac cycle. That is, the cardiac cycle length does not increase but actually decreases as the vagal stimulation frequency is raised. Background levels of sympathetic stimulation do not significantly alter the range over which this "paradoxical" response occurs. Sympathetic stimulation decreases the cardiac chronotropic response to short bursts of vagal stimuli regardless of the time in the cardiac cycle that the stimulus is given; however, it does not decrease the time from the minimum vagal chronotropic response to the subsequent atrial depolarization although the total cardiac cycle is shortened. Since sympathetic stimulation shifts the overall temporal relationship between vagal stimulation and pacemaker response, small changes in sympathetic tone may greatly alter the cardiac response to phasic vagal stimulation if the vagal stimulus is given at certain times in the cardiac cycle.

Animals↗
PubMed1980

The effects of cocaine, chlorpheniramine and tripelennamine on the cardiac responses to sympathetic nerve stimulation.

The effects of cocaine (COC), chlorpheniramine (CHL), and tripelennamine (TRI) on the cardiac responses to sympathetic neural stimulation were compared in open-chest, anesthetized dogs. The amplitudes of the chronotropic responses were not significantly altered by any of these drugs. Similarly, the amplitudes of the inotropic responses were not affected significantly by either COC or TRI, but they were increased moderately by CHL. All three drugs prolonged the inotropic and especially the chronotropic responses. CHL and TRI, in addition to being antihistaminics, are inhibitors of the neuronal uptake of norepinephrine. Therefor, the similarity of the effects of CHL, TRI, and COC on the cardiac responses to sympathetic stimulation is probably ascribable to their inhibitory activities on the neuronal uptake mechanism.

Animals↗
PubMed1980

Unifocal origin of multiform extrasystoles in concealed bigeminy.

A case of concealed bigeminy is presented in which two forms of extrasystolic complexes were evident on the ECG. One form (type B) appeared after a single conducted sinus beat, in a pattern of manifest bigeminy. The other form (type A) occurred after a sequence of more than one conducted sinus beat. The two configurations have previously been explained on the basis of different foci and mechanisms. Certain features of the ECG from our patient suggested that the two forms originated from a common site. An experimental model was developed in which the right ventricle of a dog was stimulated at sub- or suprathreshold voltages on alternate sinus beats to simulate concealed bigeminy. The ECG obtained during stimulation of a single site was remarkably similar to that recorded from the patient. We have proposed that the extrasystoles that occur after a compensatory pause may spread in a manner different from those that follow a basic cardiac cycle length. The different pattern of propagation is probably ascribable to the lengthening of the refractory period of the cardiac tissues by the compensatory pause.

Animals↗
PubMed1980

Prejunctional cholinergic modulation of adrenergic neurotransmission in the cardiovascular system.

In the heart and in the blood vessel walls, complex adrenergic-cholinergic interactions occur both prejunctionally, at the level of the autonomic nerve terminals, and postjunctionally, at the level of the responding cells themselves. The principal prejunctional interaction appears to be an inhibition of the release of norepinephrine from adrenergic nerve terminals by the acetylcholine liberated from nearby cholinergic nerve endings. This inhibitory effect is mediated by muscarinic receptors located on the postganglionic sympathetic nerve terminals. The inhibitory effect of acetylcholine on cardiac and vascular tissues are therefore achieved in part by a direct influence of the cholinergic neurotransmitter on the cardiac and vascular muscle cells, and in part by an indirect influence on sympathetic neurotransmission.

Acetylcholine↗
PubMed1980

The effects of cocaine and metanephrine on the cardiac responses to norepinephrine infusions.

In open-chest, anesthetized dogs, the effects of blocking the neuronal and extraneuronal uptake mechanisms for norepinephrine on the inotropic and chronotropic responses to norepinephrine infusion were studied. Cocaine, a neuronal uptake blocking agent, potentiated and prolonged the inotropic and chronotropic responses. The chronotropic responses were more prolonged than the inotropic responses. Conversely, metanephrine, an extraneuronal uptake blocking agent, neither potentiated nor prolonged the inotropic and chronotropic responses. Hence, it appears that the neuronal uptake mechanism plays a major role in the sympathetic regulation of the heart, but that the extraneuronal uptake mechanism plays only a minor role. A pronounced interaction between the two uptake mechanisms was observed on the tendency to prolong the inotropic and chronotropic responses, such that the effects of combined blockade were much greater than the sum of the effects produced by separate blockade of the individual uptake mechanisms. However, no such interaction was observed with respect to the magnitudes of the responses.

Animals↗
PubMed1979

Concealed extrasystoles due to Wenckebach conduction delay within the reentry loop.

Long electrocardiographic strips were analyzed from an aged patient whose heart rhythm had periods of unifocal ventricular extrasystoles with fixed coupling intervals. Periods of gradual prolongation of the coupling interval finally led to omission of a ventricular premature beat. This sequence was repetitive and is considered to be the results of reentrant extrasystoles with a 3:2 Wenckebach type of conduction delay within the reentry loop. The mechanism of concealed conduction due to overlong propagation within the reentry loop is discussed.

Aged↗
PubMed1979

Concealed quadrigeminy and quintageminy.

Electrocardiographic rhythm strips were analyzed from three patients who had frequent unifocal extrasystoles. Parasystole was excluded in all three cases. Analysis of the distributions of the numbers (S) of conducted sinus beats between extrasystoles revealed that the distributions conformed to two variants of concealed quadrigeminy (namely, the "S = 4n" and "S = 4n - 2" variants) and to one variant of concealed quintageminy (namely, the "S = 5n - 2" variant). The binomial theorem was used to test the likelihoods that these patterns of distribution of extrasystoles could occur on the basis of chance alone; the probabilities were all extremely small.

Adult↗
PubMed1979

Autonomic control of right atrial contractile strength in the dog.

The combined effects of parasympathetic and sympathetic stimulation on right atrial contractile strength were assessed in open-chest, pentobarbital-anesthesized dogs. A factorial experimental design was employed to quantify the percent changes in atrial contractile strength in spontaneously beating and paced hearts as a function of the frequencies of vagal and stellate ganglion stimulation. In 7 of 10 dogs, there was a substantial interaction between the two autonomic divisions; the sympathetically mediated inotropic effect became less pronounced as the background level of vagal stimulation increased. The relationship between stimulation frequencies and atrial contractile strength was not significnatly altered by pacing the hearts.

Animals↗
PubMed1979

Effects of repetitive bursts of vagal activity on atrioventricular junctional rate in dogs.

A stable atrioventricular (AV) junctional rhythm was produced in open-chest dogs by injecting pentobarbital into the sinus node artery. When the cervical vagus nerves were stimulated repetitively, the junctional pacemaker cells tended to become synchronized with the vagal activity. During such synchronization, the junctional rate varied directly rather than inversely with the frequency of vagal stimulation. The magnitude of the chronotropic response depended on the timing of the vagal stimuli within the cardiac cycle. In 9 dogs, when the mean heart periods were plotted as a function of the R-st intervals (i.e., the time from the beginning of ventricular depolarization to the beginning of the stimulus burst), the mean heart periods varied from a maximum of 1,815 ms to a minimum of 1,160 ms, depending on the R-st interval. A small change in the R-st interval was capable of evoking a relatively large change in cycle length. Therefore, the impulses from various efferent vagal fibers to the AV junction must arrive almost synchronously, the released acetylcholine must be removed rapidly, and the sensitivity of the pacemaker cells to acetylcholine must change rapidly at some critical time during the cardiac cycle.

Acetylcholine↗
PubMed1979

The effects of cocaine and metanephrine on the cardiac responses to sympathetic nerve stimulation in dogs.

The effects of infusions of cocaine (COC) and metanephrine (MET) on the inotropic and chronotropic responses to cardiac sympathetic nerve stimulation were studied in open-chest, anesthetized dogs. COC blocks the neuronal uptake of norepinephrine (NE), whereas MET blocks the extraneuronal uptake. Both blocking agents slightly enhanced the inotropic but not the chronotropic responses. COC prolonged the cardiac responses significantly, particularly the chronotropic responses, whereas MET had no appreciable effect on the durations of these responses. Hence, it appears that the neuronal uptake mechanism plays a major role in the dissipation of neurally released NE in the heart, but that the extra-neuronal uptake mechanism plays only a minor role in its dissipation. In contrast to the results in certain other tissues, the combined effects of COC and MET on the cardiac responses were no greater or more prolonged than the sum of the effects produced by each agent acting alone.

Analysis of Variance↗
PubMed1978

The influence of cocaine and desipramine on the cardiac responses to exogenous and endogenous norepinephrine.

In open-chest, anesthetized dogs, cocaine and desipramine potentiated the pressor, chronotropic, inotropic and coronary sinus blood flow responses to norepinephrine (NE) infusions. The chronotropic and inotropic responses were also prolonged, the former more markedly than the later and the extraction of exogenous NE from the coronary blood stream was diminished. Cocaine and desipramine also potentiated the pressor and coronary sinus blood flow responses, but not the chronotropic or inotropic responses, to stimulation of the left ansa subclavia. The inotropic response was slightly prolonged, however, and the chronotropic response was markedly prolonged. The overflow of NE into the coronary sinus blood was not increased by either neuronal uptake blocking agent. It is proposed that cocaine and desipramine, at the doses employed, diminish the release of NE from the cardiac nerve endings at the same time that they inhibit reuptake of the neurotransmitter. Their mechanisms of action and their side effects on the circulatory system do not appear to differ significantly.

Animals↗
PubMed1978

Concealed atrial bigeminy and trigeminy.

Patterns indicative of concealed atrial extrasystoles were observed in two patients with frequent premature atrial depolarizations. In the first patient, the predominant pattern was such that most of the numbers (S) of sinus P waves between atrial extrasystoles satisfied the equation S = 3n-1, where n is any positive integer. This pattern is characteristic of concealed trigeminy. Over a sequence of 49 interectopic intervals, this patient vacillated between concealed atrial trigeminy and bigeminy. A second patient displayed a pattern characteristic of the "even number" variant of concealed bigeminy. The numbers of sinus P waves in consecutive interectopic intervals were predominantly even. These various patterns of concealed atrial extrasystoles closely resemble previously reported patterns of concealed ventricular extrasystoles.

Aged↗
PubMed1978

Autonomic control of pacemaker activity in the atrioventricular junction of the dog.

A stable atrioventricular (AV) junctional rhythm was induced in open-chest, anesthetized dogs by injecting pentobarbital into the sinus node artery. A factorial experimental design was used to quantify the changes in AV junctional rate as a function of the frequency of cardiac sympathetic and parasympathetic stimulation. The AV junctional pacemaker cells were more responsive to autonomic neural stimulation, but the vagal-sympathetic interactions were less pronounced than had previously been observed for the SA nodal pacemaker cells. In a group of seven animals, sympathetic stimulation at a frequency of 1.4 Hz increased the AV junctional rate by 102% from a control rate of 54 beats/min. In the same animals, vagal stimulation at a frequency of 8.4 Hz reduced the AV junctional rate by 56%. In three other animals, the AV junction was even more responsive; equivalent chronotropic effects were achieved with stimulation frequencies that were only about one-third of those cited above. There was a moderate, but significant, autonomic interaction: in the group of seven animals, the positive chronotropic effect of sympathetic stimulation at 1.4 Hz was 72% greater at the low level (0 Hz) than at the high level (8.4 Hz) of vagal activity.

Animals↗