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Biomedical subjects

M B Waxman

Publications and source records attributed to M B Waxman.

At least 19 recordsLinked to original sources
PubMed1992

Vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol.

UNLABELLED: Testing for the susceptibility for vasodepressor reaction in humans involves the combination of restriction of venous return by passive upright tilting and the administration of isoproterenol. To explore the basis of the vasodepressor test in humans, the present experiment examined whether a reduced cardiac volume coupled with adrenergic stimulation causes a vasodepressor reaction in rats. Vasodepressor reaction was defined as paradoxical heart rate slowing in conjunction with hypotension during inferior vena caval occlusion. Inferior vena caval occlusion was performed for 60 s and the maximum changes in R-R were measured during seven states as follows. (A) Under control conditions inferior vena caval occlusion alone accelerated the rate in 32 of 32 rats (delta R-R, -13.9 +/- 1.7 ms, p less than 0.001). (B) When inferior vena caval occlusion was performed during an infusion of isoproterenol (0.5-1.0 micrograms.min-1), a vasodepressor reaction was observed in all rats as the heart rate slowed (delta R-R, +138.1 +/- 14.8 ms, p less than 0.001). The vasodepressor reaction was further examined during isoproterenol and inferior vena caval occlusion under five additional states. (C) After atropine the vasodepressor reaction was unchanged (delta R-R, +132.7 +/- 24.8 ms, p less than 0.001). (D) After bilateral vagotomy the paradoxical slowing was eliminated. (E) After intrapericardial lidocaine the paradoxic slowing was eliminated. (F) After bilateral stellectomy nonsignificant slowing was still present, but this was markedly reduced when compared with B (p less than 0.001). (G) Following chronic chemical sympathetic denervation with 6-hydroxydopamine the paradoxic bradycardia was eliminated. CONCLUSIONS: (1) Reduced cardiac volume combined with adrenergic stimulation can stimulate a vasodepressor reaction; (2) the vasodepressor reaction requires signalling by the afferent but not efferent vagal fibers; (3) the bradycardia is mainly due to withdrawal of sympathetic efferent tone.

Animals↗
PubMed1992

Localization of the reflex pathway responsible for the vasodepressor reaction induced by inferior vena caval occlusion and isoproterenol.

Vasodepressor reactions were induced in 27 rats by a combination of inferior vena caval occlusion and an infusion of isoproterenol. A vasodepressor reaction was defined as paradoxical heart rate slowing during inferior vena caval occlusion. The R-R intervals were measured at 5-s intervals before, during, and after 60 s of inferior vena caval occlusion. The purpose of this study was to examine the role of the right and left vagus nerve and the right and left stellate ganglia in this reflex. Under control conditions inferior vena caval occlusion accelerated the rate (R-R, -15.9 +/- 0.9 ms). During an infusion of isoproterenol (0.5-1.0 micrograms.min-1), inferior vena caval occlusion produced paradoxical rate slowing, i.e., a vasodepressor reaction (R-R, +75.0 +/- 2.2 ms). The vasodepressor reaction was examined during inferior vena caval occlusion and isoproterenol under the following additional states: atropine methyl bromide or right vagotomy did not alter the reaction; left vagotomy eliminated the reaction; and right or left stellectomy greatly reduced the vasodepressor reaction. We conclude the following: (1) left vagal afferents mediate the vasodepressor reaction; (2) cardiac sympathetic fibers participate in the vasodepressor reaction by withdrawing efferent tone through the right stellate ganglion, and by generating the afferent signal, which triggers the vasodepressor reaction through the left stellate ganglion.

Animals↗
PubMed1992

The effects of sympathetic denervation on spontaneous ventricular defibrillation in the rat.

Ventricular tachycardia or ventricular fibrillation was electrically induced in 38 normal rats (group 1) and 24 sympathetically denervated rats (6-hydroxydopamine) (group 2). The time for spontaneous reversion to sinus rhythm was measured during (1) control, (2) isoproterenol, and (3) the combination of isoproterenol and phenylephrine. The time for spontaneous reversion was the same in both groups in the three states. The reversion time was prolonged threefold by isoproterenol, and restored to control values when phenylephrine was added to the infusion of isoproterenol. The tachycardia duration and the refractory period were inversely related: log10 (tachycardia duration) = 3.466-0.091 (refractory period). Ventricular tachycardia/fibrillation induction was examined as follows: (i) Ventricular tachycardia/fibrillation was induced in 100% of normal rats (group 1), but only 42% of the denervated rats (group 2, p less than 0.001); (ii) during isoproterenol, ventricular tachycardia/fibrillation was induced in 100% of rats of both groups; and (iii) when phenylephrine was added to isoproterenol, ventricular tachycardia/fibrillation was induced in 100% of group 1 rats versus 82% of group 2 rats, (p = NS). These observations suggest (1) the induction of ventricular tachycardia/fibrillation is highly dependent on intact sympathetic innervation, and (2) exogenous adrenergic agonists modulate the duration of ventricular fibrillation through their effects on ventricular refractory period, independent of sympathetic innervation.

Animals↗
PubMed1991

Effects of posture, Valsalva maneuver and respiration on atrial flutter rate: an effect mediated through cardiac volume.

The effects of passive upright tilting from 0 degrees to +60 degrees (n = 27), Valsalva maneuver (n = 16) and respiration (n = 10) on the rate of atrial flutter were studied in 27 patients. After tilting to +60 degrees, the atrial flutter cycle length shortened in all patients from 247.5 +/- 7 to 236.7 +/- 6.9 ms (range of shortening 1 to 21 ms, p less than 0.001). The Valsalva maneuver (strain of 40 mm Hg) shortened the flutter cycle length during the strain (phase 2) from 242.2 +/- 4.6 to 230.5 +/- 5 ms (range of shortening 2 to 19 ms, p less than 0.001). In 10 patients whose respiration was monitored, the flutter cycle length consistently prolonged during inspiration and shortened during expiration. Combined beta-adrenergic and muscarinic receptor blockade in six patients did not significantly alter the flutter cycle length at rest or the effects of the various maneuvers on the changes in flutter cycle length. This study revealed that the atrial flutter cycle length can be shortened by passive upright tilting, the strain phase of the Valsalva maneuver and expiration. Changes in flutter cycle length were independent of autonomic tone, implying that by decreasing cardiac volume, these maneuvers affect characteristics of the atrial flutter circuit, thereby producing dynamic changes in the rate of atrial flutter.

Atrial Flutter↗
PubMed1990

The mechanism of flutter interval alternans.

The mechanism of atrial flutter alternans was investigated by observing the effects of ventricular systole on flutter intervals in a patient with atrioventricular dissociation. Interval measurements were made both from atrial electrograms recorded from an esophageal electrode, and from surface ECG recordings. Flutter cycle intervals that occurred during a well-defined period subsequent to ventricular systole were consistently prolonged by up to 30 msec relative to the baseline flutter cycle interval. This prolongation was observed in two vastly different electrode configurations, implying that motion artifact was not predominantly responsible. We concluded that, by altering the characteristics of the flutter reentry circuit, transient increases in atrial volume and/or pressure arising during ventricular systole were responsible for the lengthening of the flutter cycle intervals.

Adult↗
PubMed1990

Cardiac innervation after double lung transplantation. Toronto Lung Transplant Group.

Double lung transplantation has been successfully introduced for patients with end-stage pulmonary disease and preserved cardiac function. An advantage of this operation compared with heart-lung transplantation is retention of the recipient's heart. The operative dissection, however, may lead to interruption of sympathetic and parasympathetic pathways to the heart and consequent denervation of the native heart. The cardiac innervation of seven double lung transplant recipients was investigated by the heart rate response to carotid sinus massage, the Valsalva maneuver, intravenous injection of atropine, and exercise. Five single lung and two heart-lung transplant recipients were studied for comparison. Of the seven double lung transplant recipients, three had abnormal responses to carotid sinus massage, six to the strain phase of the Valsalva maneuver, and five to the release phase of the Valsalva maneuver. Three of six double lung transplant recipients tested had no response to intravenous injection of atropine, and five of seven patients had an abnormal recovery of heart rate after maximal exercise. No patient had a normal response to all interventions, and three patients had responses compatible with complete cardiac denervation. It is concluded that cardiac denervation may occur after double lung transplantation, most likely caused by surgical interruption of sympathetic and parasympathetic pathways during dissection of the recipient's trachea.

Adult↗
PubMed1989

Isoproterenol induction of vasodepressor-type reaction in vasodepressor-prone persons.

The ability of isoproterenol to induce symptoms and laboratory findings of a vasodepressor reaction was tested in 48 patients, ages 17 to 74, divided into 4 groups according to the reason for their referral. Group 1 comprised 12 patients with vasodepressor syncope, group 2 had 8 patients with syncope of unknown origin, group 3 included 11 patients with syncope due to seizures in 2 and ventricular tachycardia in 9, group 4 had 17 patients with various arrhythmias not associated with syncope. Isoproterenol boluses were administered starting at 2 micrograms and increased in 2-micrograms steps to a maximum of 8 micrograms at 0 degree and +60 degrees. The responses at 0 degrees were all normal. At +60 degrees a vasodepressor reaction consisting of syncope or near syncope, hypotension and bradycardia was produced by isoproterenol (mean dose 6.0 +/- 0.26 micrograms) in 8 patients from group 1 (66.6%), 4 from group 2 (50%), 0 from group 3 and 4 from group 4 (23.5%). Three of the 4 patients in group 4 had a remote history of classic vasodepressor syncope. The overall sensitivity and specificity of the test were 73 and 85%, respectively, while the predictive accuracy of a test with positive or negative outcome were 69 and 89%, respectively. Muscarinic receptor blockade with atropine in 4 patients prevented isoproterenol-induced bradycardia but not hypotension or symptoms of fainting. Beta-adrenergic receptor blockade with propranolol inhibited all aspects of the isoproterenol-induced faint. Thus, the administration of isoproterenol during a passive upright tilt may identify persons who suffer from or are prone to a vasodepressor reaction.

Adult↗
PubMed1989

The protective effect of vagus nerve stimulation on catecholamine-halothane-induced ventricular fibrillation in dogs.

Parasympathetic neural activity modulates some ventricular arrhythmias in man. Therefore, a canine model of arrhythmias produced by the interaction of halothane and catecholamines was used to study the effects of vagal stimulation on the induction of ventricular fibrillation. The dose of catecholamine required to induce ventricular fibrillation was determined during a constant heart rate. Vagal stimulation reversibly raised the norepinephrine dose that produced ventricular fibrillation from 16.4 +/- 2.4 to 30.0 +/- 3.8 micrograms (p less than 0.001, n = 10), and the epinephrine dose from 15.5 +/- 2.0 to 22.5 +/- 2.6 micrograms (p less than 0.001, n = 5). Following atropine, vagal stimulation failed to raise the threshold dose of norepinephrine (16.8 +/- 2.4 vs. 18.3 +/- 3.3 micrograms, nonsignificant, n = 6) or epinephrine (15.5 +/- 2.0 vs. 16.0 +/- 2.3 micrograms, nonsignificant, n = 5). Ligation of the cervical vagus nerves did not affect the epinephrine threshold dose (16.3 +/- 3.3 vs. 17.5 +/- 2.7 micrograms, nonsignificant, n = 5). Following elevation of basal vagal tone by morphine premedication, the norepinephrine threshold of 53.0 +/- 9.2 micrograms declined by a nonsignificant amount to 46.5 +/- 11.5 micrograms after vagotomy (nonsignificant, n = 5). Thus resting vagal tone does not prevent catecholamine-halothane-induced ventricular fibrillation, whereas increasing vagal tone by electrical stimulation substantially protects against this arrhythmia. The protection is mediated through a muscarinic cholinergic receptor.

Animals↗
PubMed1988

Modulation of an idioventricular rhythm by vagal tone.

A 28 year old man with a stable permanent idioventricular rhythm of 80 to 85 beats/min, with all the characteristics of a pacemaker, is described. This pacemaker was slowed by maneuvers that enhanced vagal tone, including carotid sinus massage, the postrelease phase of the Valsalva maneuver and phenylephrine. The pacemaker was also slowed by a cholinesterase inhibitor (edrophonium hydrochloride) and accelerated by a muscarinic receptor blocking drug (hyoscine butylbromide). The actions of these maneuvers and agents were independent of sympathetic tone as propranolol pretreatment did not alter their effects. Similarly, propranolol did not affect the pacemaker rate. The pacemaker was not dependent on a slow inward current because verapamil did not affect its rate. The pacemaker accelerated in response to increased sympathetic tone induced by exercise and upright tilting and to the adrenergic agonist isoproterenol. The pacemaker was localized to the high posterior septal region of the left ventricle underneath the mitral valve. This report describes in a man an idioventicular pacemaker that is innervated by sympathetic and vagal fibers and responsive to alterations in tone of both limbs of the autonomic nervous system. It offers the first clear proof that a ventricular pacemaker can be innervated and controlled by the vagus nerve and provides its location.

Adult↗
PubMed1986

Spontaneous termination of paroxysmal supraventricular tachycardia following disappearance of bundle branch block ipsilateral to a concealed atrioventricular accessory pathway: the role of autonomic tone in tachycardia diagnosis.

We present a case of an 18-year-old man with a history of palpitations in whom episodes of paroxysmal supraventricular tachycardia were easily initiated by administered atrial premature beats. In all 15 control episodes of tachycardia, functional left bundle branch block (LBBB) seen at the onset, resolved within 10-20 cycles (mean, 13.1 +/- 0.95). The tachycardia ended with the normalized QRS complex in each episode. Eleven episodes ended because of block within the antegrade pathway (ended with a P-wave), and four episodes stopped because of block within the retrograde pathway (ended without a P-wave). During the administration of isoproterenol (1 mg/min IV) all six episodes of tachycardia had LBBB but these did not end when LBBB disappeared spontaneously. When LBBB subsided, the mean tachycardia cycle interval shortened from 328.5 +/- 1.4 to 264.2 +/- 2.1 ms (p less than 0.001). Each episode of tachycardia was then terminated by carotid sinus massage. The disappearance of LBBB in control conditions presented the retrograde and antegrade limbs of the reentrant circuit with an early impulse that stopped the tachycardia. After isoproterenol administration, the tachycardia did not end following disappearance of LBBB, thus enabling the tachycardia cycle interval to shorten by a mean of 64.3 +/- 1.9 ms. This extent of tachycardia acceleration is diagnostic of the participation of a concealed, left free-wall bypass tract.

Adolescent↗
PubMed1985

[In vitro electrophysiological effects of sodium dantrolene on isolated preparations of Purkinje fibers and ventricular myocardium of sheep].

Dantrolene sodium is a drug used in the treatment of spasticity and malignant hyperthermia. It is known to have a myorelaxant effect related to inhibition of the "release" of calcium by the sarcoplasmic reticulum of striated skeletal muscle. A direct cardiac effect which has only recently been suspected was demonstrated in vitro on isolated preparations of sheep Purkinje fibres and ventricular myocardium. Dantrolene caused a spectacular lengthening of the duration of the action potential of Purkinje fibres. This could be due either to an action on the slow calcium current or to stimulation of an ingoing sodium current sensitive to tetrodotoxin (TTX). This effect on the cardiac action potentials could explain the antiarrhythmic properties of dantrolene sodium during attacks of malignant hyperthermia.

Action Potentials↗
PubMed1979

Management of intractable ventricular tachyarrhythmias after myocardial infarction.

Twenty-five patients with recent or old myocardial infarction were studied because they had life-threatening ventricular arrhythmias that required repeated cardioversions and were intractable to medical management. All patients had had a large anterior infarction a mean of 4.6 weeks before the emergence of the arrhythmias and all had severe left ventricular dysfunction. Cardiac catheterization or autopsy revealed a left ventricular aneurysm in 18 of 18 patients and obstruction of the left anterior descending coronary artery in 20 of 20 patients. Of 16 patients treated surgically with aneurysm resection or coronary bypass grafting, or both, 10 (62 percent) were alive after 3 to 39 (mean 26) months of follow-up. The perioperative mortality rate was 31 percent and only one patient died during the postoperative follow-up period 4 months after discharge from the hospital. By contrast, all nine medically treated patients died either in the hospital (four patients) or suddenly within 2 months of discharge (five patients). Ventricular fibrillation was documented as the cause of death in five of these patients. Surgical intervention was found to improve significantly the survival of these patients (P less than 0.02). The perioperative mortality rate was lower when at least 4 weeks had elapsed from acute infarction to surgery (10 versus 67 percent) and when the procedure included coronary bypass grafting (13 versus 50 percent), although these differences were not statistically significant (P greater than 0.05).

Adult↗
PubMed1979

Carotid sinus massage induced elimination of rate related bundle branch block during paroxysmal atrial tachycardia: a simple method of proving bypass tract participation in the tachycardia.

Four cases of paroxysmal atrial tachycardia are described in whom rate related left bundle branch block (LBBB) was often present which persisted indefintely and showed no signs of spontaneous disappearance. Transient slowing of the tachycardia by carotid sinus massage in each case eliminated LBBB and this led to tachycardia acceleration. The tachycardia acceleration was traceable to a shortening in ventriculoatrial conduction. These observations proved the participation of a left sided bypass tract in the tachycardia circuit in each of these cases.

Bundle-Branch Block↗
PubMed1979

Autonomic pathways responsible for bradycardia on facial immersion.

The autonomic pathways mediating the bradycardia response to facial immersion (FI) have not been fully elaborated in man. By means of parasympathetic and sympathetic blockade we studied the heart rate response to FI in nine highly trained young swimmers, at rest and during dynamic cycle exercise. With no blockade, heart rate at rest declined with FI 36 +/- 18%. Under beta-blockade with propranolol or alpha-blockade with phentolamine FI produced a similar decrement. Atropine reduced the response. During exercise FI produced 48 +/- 9% decline without blockade. The response was similar with beta-blockade, but was completely abolished with atropine. Systolic blood pressure responses to FI measured by cuff in three subjects were small and bore no relation to the heart rate response. The results are compatible with parasympathetic efferent mediation of the heart rate response to FI. They are incompatible with a role for sympathetic mediation except as a complex interaction between parasympathetic and sympathetic influences. Hypertension and other sympathetic responses to FI do not play a role in production of bradycardia, but are apparently incidental effects. The heart rate decrement produced by FI increases with greater steady-state heart rate.

Adolescent↗