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Biomedical subjects

J M Loeb

Publications and source records attributed to J M Loeb.

At least 55 records · Page 3Linked to original sources
PubMed1984

Operative therapy for ventricular arrhythmia.

The history of surgical attempts to control ventricular arrhythmia is reviewed and current methodology is presented in detail. The results of the various surgical approaches and future trends in the management of this troublesome condition are discussed.

Arrhythmias, Cardiac↗
PubMed1984

Postvagal potentiation of the chronotropic effect of norepinephrine.

Following termination of vagal stimulation, heart rate increases above control (postvagal tachycardia). This phenomenon has been attributed to vagally mediated release of norepinephrine in the sinus node region, although other contributory factors may be important. The possibility that, during the postvagal period, the chronotropic efficacy of norepinephrine is enhanced was investigated. Mongrel dogs (N = 6) were pretreated with reserpine in order to minimize postvagal tachycardia and hence allow reliable detection of enhanced responsiveness to norepinephrine. The dogs were then anesthetized with chloralose, autonomically decentralized, and instrumented to record electrocardiogram, aortic blood pressure, and electrograms from right atrium and right ventricle. Thirty-, forty-, or sixty-second infusions of norepinephrine were administered via the sinus node artery. The mean cycle length decrease produced by norepinephrine alone was 95 msec (which corresponds to a heart rate increase of + 19.6 bpm). After a 30-sec period of vagal stimulation, norepinephrine infusions produced a cycle length decrease of 139 msec (+32.5 bpm). These results are significant at the P less than 0.05 level. It is concluded that norepinephrine infusions produce a significantly greater magnitude of tachycardia when administered postvagally. It is proposed that this postvagal potentiation of the chronotropic effect of norepinephrine may contribute to postvagal tachycardia. Indeed, there may be a synergistic relationship between this phenomenon and vagally mediated release of norepinephrine in the mediation of postvagal tachycardia.

Animals↗
PubMed1984

Autoregulation of cardiac cycle length: role of catecholamines.

The mechanism of autoregulation of cardiac cycle length during phasic alterations in perfusion via the sinus node artery is unclear. Inasmuch as transient catecholamine release has been documented during sinus node artery injections, we sought to determine whether autoregulation of cycle length might be related to a beta receptor-mediated process. We used chloralose-anesthetized mongrel dogs. A right thoracotomy was performed, the vagi and sympathetic inputs to the heart were cut and electrograms were recorded from the sinoatrial (SA) node, right atrium, right ventricle and His bundle. The SA node artery was catheterized and distribution verified. Perfusion of normal Tyrode's solution via the SA node artery at 3 ml/min resulted in significant cycle length slowing which was maximal immediately after onset of perfusion. Plots of the derivative of cycle length with respect to time indicated either a monophasic or biphasic pattern of response. Administration of propranolol (2 mg/kg i.v.) resulted in a significant prolongation of control cycle length. Perfusion of normal Tyrode's solution after propranolol resulted in significantly greater degrees of cycle length prolongation (as judged by integration of area under cycle length curves) as well as only monophasic response patterns. These results suggest that infusions of normal Tyrode's solution, via the SA node artery, at physiologic flow rates are accompanied by concurrent catecholamine release throughout the infusion. This catecholamine release may contribute to the homeostatic regulation of cardiac cycle length.

Animals↗
PubMed1983

Operative therapy of malignant ventricular rhythm disturbances.

Pre- and postoperative electrophysiologic study (EPS), intraoperative cardiac mapping, and extended endocardial resection of scar (EER) has enabled us to identify subgroups among 94 patients who have had operation to control or prevent malignant ventricular arrhythmia. Operative mortality was 8.5% and cure or prevention of ventricular arrhythmia was accomplished in 92% of survivors. Group 1: 13 patients were resuscitated from "sudden death" due to ventricular fibrillation (VF). All had exercise-induced VF and/or ventricular tachycardia (VT). Preoperative EPS revealed no inducible VT/VF. All had coronary artery disease, without evidence of myocardial infarction (MI) or ventricular wall motion abnormality; all were cured with conventional myocardial revascularization. Group 2: 65 patients had MI with residual left ventricular wall motion abnormality, usually aneurysm. The malignant arrhythmia, either sustained VT (38 patients) or VF (27 patients), was inducible by EPS but not usually by exercise, and all were refractory to medical therapy. Treatment was operative mapping, aneurysmectomy, EER, and coronary revascularization. Operative mortality was 11.9%; 90% of survivors are arrhythmia free, off drugs; 10% are now drug responsive. Group 3: 3 patients without coronary disease had VT or VF caused by endocardial sarcoidosis or operative scar from a previous congenital heart operation. Treatment was EPS, operative mapping, and excision of abnormal endocardial scar with no operative mortality. Group 4: 13 patients underwent aneurysmectomy for indication other than arrhythmia, but had preoperative ventricular irritability which was not life-threatening. Operation was aneurysmectomy, prophylactic EER, and revascularization with no mortality and no postoperative arrhythmic events. After many years of unpredictable and unsatisfactory results from various empirical surgical approaches, the operative treatment of malignant ventricular arrhythmia is now based on sound electrophysiologic principles.

Arrhythmias, Cardiac↗
PubMed1982

Differential cholinergic sensitivity of sinus and AV nodes.

The effects of the muscarinic antagonist gallamine were studied in anesthetized dogs via selective perfusion of the SA and AV nodal arteries. Before gallamine, acetylcholine injected into the SA node artery induced asystole while injection into the AV node artery induced heart block. After gallamine, acetylcholine via the AV node artery was without effect while, via the SA node artery, acetylcholine still induced negative chronotropic effects. Thus the muscarinic receptors of the SA and AV nodes may be inhomogeneous.

Animals↗
PubMed1982

Extended endocardial resection for the treatment of ventricular tachycardia and ventricular fibrillation.

A total of 40 patients with drug-refractory, life-threatening cardiac rhythm disturbances--ventricular tachycardia in 23 patients and ventricular fibrillation in 17 patients--underwent extended endocardial resection (EER) of scar tissue. Scarring was due to myocardial infarction in 38 patients, to previous congenital heart operation in 1 patient, and to sarcoidosis of the heart in 1. The EER procedure was directed by epicardial and endocardial mapping data whenever possible, and was usually combined with revascularization, aneurysmectomy, or, in 5 patients, mitral valve replacement. Operative mortality was 10%, incident to poor preoperative ventricular function and hemorrhage secondary to previous cardiac surgical procedures. Thirty-three of the 36 survivors (92%) are free of arrhythmia at follow-up periods ranging from 3 to 36 months (mean, 12.5 months); the arrhythmia in the remaining 3 patients is now drug controlled. Thirty-three patients had postoperative electrophysiological studies, and in 30 (91%), the arrhythmia was no longer inducible. The results of surgical treatment for ventricular tachycardia and ventricular fibrillation were similar. The results also proved satisfactory whether the EER procedure was directed by visual observation or mapping.

Adolescent↗
PubMed1982

Sinus node in SIDS.

Explore the source record for details and available documents.

Coronary Circulation↗
PubMed1981

Autonomic interactions among subsidiary atrial foci.

Although the existence of a specific pacemaker hierarchy outside of the sinus node but within the atrium has been documented, little evidence regarding mechanisms controlling activity of these sites has been gathered. This investigation utilized an autologous perfusion of the sinus nodal artery, by way of the femoral artery, in order to suppress the sinus node cholinergically while unmasking latent atrial sites. Electrograms were recorded from the region of the sinus node and several atrial sites. Perfusion with small doses of acetylcholine and physostigmine unmasked pacemakers outside of the sinus and atrioventricular nodes, but within the atrium. Either vagal stimulation or topical acetylcholine on the area of the presumed pacemaker returned dominance gradually toward the sinus node. Stimulation of the right stellate ganglion accelerated the latent pacemaker but did not shift activation toward the sinus node. These results are consistent with the existence of subsidiary atrial pacemakers that appear to be highly sensitive to the effects of acetylcholine. This may represent one mechanism, in addition to overdrive suppression, that maintains pacemaker hierarchy within the right atrium.

Acetylcholine↗
PubMed1981

Accuracy in coronary graft flow measurement.

A blood flow calibration apparatus is described for use with electromagnetic flow probes. It is an automatic gravity-flow system, which provides a constant level and therefore constant flow at any preset rate. On several occasions, the use of this device has helped to determine whether flow probes require simple adjustment, factory repair, or replacement. Using this system, a systematic error in the manufacturer's "precalibration" averaging +22% (range, 9 to 50%) has been discovered, and appropriate corrections have been made. The accuracy of these corrections has been confirmed by a rapid, in vivo method of calibration, which also is described and which can be carried out during the conduct of aortocoronary bypass operation. It is recommended that all groups measuring coronary graft flow become familiar with their electromagnetic flowmeter and probes by means such as those described, in the interest of accurate flow measurement after bypass operation.

Blood Flow Velocity↗
PubMed1981

Sensitivity differences of SA and AV node to vagal stimulation: attenuation of vagal effects at SA node.

The present study sought to characterize vagally induced desensitization at the sinoatrial (SA) node of the intact dog and to determine whether these findings could be extended to atrioventricular (AV) Nodal conduction. Autonomically decentralized anesthetized dogs were instrumented to record electrocardiograms, arterial pressure, and electrograms from the SA node, right atrium, right ventricle, and His bundle. During right- or left-vagal stimulation for 60 s, cycle length (CL) increased initially, followed by a gradual recovery toward control during stimulation; atrio-His (AH) interval remained prolonged throughout the stimulation. Atrial drive increased AH interval during stimulation, but AH prolongation was maintained throughout the stimulation period. To rule out acetylcholine (ACh) depletion, ACh was administered before and during vagal stimulation. Although control CL and AH interval were lengthened by ACh, no significant CL increases occurred when ACh was given during stimulation, but the AH interval became longer. Propranolol increased control CL and AH interval but did not alter the relationship between vagal stimulation and CL or AH interval. Thus the negative chronotropic effect of ACh at the SA node is diminished upon prolonged vagal stimulation, whereas the negative dromotropic effect upon AV nodal conduction remains unaltered. These results suggest differences in muscarinic receptor behavior at the SA and AV nodes.

Acetylcholine↗
PubMed1981

Suppression or enhancement of natural killing does not alter tolerance to bovine gamma globulin.

NZB/NZW F1 (B/W) mice have high levels of natural killing (NK), are resistant to the induction of tolerance to bovine gamma globulin (BGG), and spontaneously develop a disease resembling systemic lupus erythematosus. In vivo administration of 89Strontium (89Sr) to B/W mice reduces NK and improves their autoimmune disease. We tested the hypothesis that the high levels of NK exert an immunoregulatory influence and are responsible for the resistance to BGG tolerance. 89Sr was administered at 4 and 8 weeks, and tolerogen was injected at 10 weeks. Despite a marked suppression of NK, 89Sr-treated B/W mice remained resistant to the induction of tolerance. NK was stimulated in weanling B/W male and female mice, and in adult A/J females, by the injection of Poly I . C one day prior to the administration of tolerogen. Poly I . C induced an acute rise in NK but did not inhibit the induction of tolerance. We conclude that natural killer cells are not involved in the regulation of immune tolerance to BGG and, they do not appear to play a role in the resistance to tolerance in adult B/W mice.

Age Factors↗
PubMed1980

Cardiac arrhythmias after chronic embolization of the sinus node artery: alterations in parasympathetic pacemaker control.

Embolization of the sinus node artery was accomplished in dogs by injecting rapidly hardening vinyl latex into the sinus node artery. Embolization immediately shifted the pacemaker to a junctional focus; however, with time postoperatively, the pacemaker shifted to an atrial site. Variable episodes of pacemaker failure, sinoatrial block, junctional rhythm, wandering atrial pacemaker and idioventricular escape rhythms were commonly observed on Holter monitor in isolation but only rarely when the dog was in the laboratory. Severe bradycardia (38.9 +/- 3.7 beats/min) was the predominant rhythm by 3-6 months postoperatively. In addition, these same dogs had a greater overall increase in heart rate after atropine than normal dogs (17.5 +/- 13.5 vs 116.6 +/- 15.9 beats/min above control; p less than 0.02). Responses to vagal stimulation in this group were abnormal, as long periods of asystole and bradycardia were observed after stimulation was terminated. These data suggest an alteration in parasympathetic pacemaker control after chronic embolization of the sinus node artery.

Animals↗
PubMed1979

Supraventricular pacemaker underdrive in the absence of sinus nodal influences in the conscious dog.

The ability to reduce and maintain heart rate by electrical stimulation (underdrive) was tested in three groups of chronically instrumented dogs: sinoatrial node intact, ectopic atrial pacemaker produced by injection of rapidly hardening latex into the sinoatrial nodal artery, and idioventricular pacemaker produced by injection of formalin into the atrioventricular node. In the conscious unsedated state, underdrive of sinoatrial or idioventricular pacemakers resulted in competition between driven and intrinsic foci. However, the cycle length of ectopic atrial pacemakers could be increased by 148.4 +/- 30.7 msec (P less than 0.001) and maintained at that value. Cessation of underdrive resulted in a period of pacemaker suppression similar to that produced following overdrive. Single premature stimuli produced marked cycle length prolongations in dogs with ectopic atrial foci. Total autonomic blockade had no significant effect on the production of underdrive. Thus, the results of the present experiments provide evidence for maintained capture of cardiac pacemakers at rates significantly below intrinsic control and indicate that underdrive varies as a function of pacemaker site. Underdrive may explain the failure of junctional escape in the presence of slower atrial rhythms.

Animals↗