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Biomedical subjects

B Lown

Publications and source records attributed to B Lown.

At least 217 records · Page 12Linked to original sources
PubMed1976

Differing mechanisms for ventricular vulnerability during coronary artery occlusion and release.

The time course and mechanism of vulnerability to ventricular fibrillation (VF) a 10-minute occlusion of the left anterior descending coronary artery and following its release were studied in 48 dogs. VF threshold was determined by inducing a sequence of three extrasystoles (sequential R/T pulsing). Within 1 minute of occlusion, the fibrillation current decreased to the level required for eliciting a propagated diastolic response. This state of enhanced vulnerability lasted for approximately 6 minutes, after which the VF threshold returned to preocclusion values. The vulnerability changes upon reperfusion, by comparison, occurred within seconds of release and persisted only transiently. Three minutes of occlusion was the minimal time which resulted in a reduction in VF threshold after release. Alpha and beta-adrenergic blockade with phentolamine and propranolol, respectively, prevented the decrease in VF threshold during occlusion but were without effect upon threshold changes during coronary artery release. Lidocaine failed to alter the pattern of vulnerability. It is concluded that adrenergic mechanisms play a key role in the increased susceptibility to VF associated with acute myocardial ischemia, whereas the changes in VF threshold following reperfusion may be due to washout products of cellular ischemia. These findings support the view that protection against VF during coronary artery occlusion and release may require different antiarrhythmic measures.

Animals↗
PubMed1976

Coronary occlusion before, during, and after strenuous exercise.

Groups of dogs were exercised immediately before, and immediately after occlusion of the left anterior descending coronary artery. Coronary occlusion by a staged procedure resulted in a low mortality and rare ventricular ectopic beats. The combination of simultaneous exercise with coronary occlusion reproducibly provoked ventricular fibrillation (VF). Exercise before and after occlusion frequently produced ventricular tachycardia but no VF. The risk of major arrhythmias was related to the peak heart rate resulting from the exercise.

Animals↗
PubMed1976

Repetitive extrasystole as an index of vulnerability to ventricular fibrillation.

The assessment of ventricular vulnerability by inducing ventricular fibrillation (VF) presents limitations when neural activity is being investigated, especially in the unanesthetized animal. As repetitive extrasystoles (RE) have been observed to precede the occurrence of VF, it was relevant to determine whether the RE threshold provides a reliable index of cardiac susceptivility to fibrillation. The RE and VF threshold relationships were studied in 32 chloralose-anesthetized dogs during left stellate ganglion stimulation, vagus nerve stimulation, and beta-adrenergic blockage with practolol. The vulnerable period was scanned at 1-ms intervals and at 2-mA increments with a single, 2-ms, constant-current cathodal stimulus; RE and multiple RE were induced reproducibly when 66% and 82%, respectively, of the fibrillatory current was administered. The nadirs for RE and multiple RE were coincident in the cardiac cycle with the vulnerable-period threshold for VF. Stellate and vagal stimulation and beta-adrenergic blockade resulted in comparable changes in RE and VF thresholds and produced equivalent shifts in the cardiac cycle of the RE and VF vulnerable-period nadirs. These observations suggest that RE and VF phenomena share a common electrophysiologic basis and that the RE threshold can be used as an end point for measuring ventricular vulnerability to VF.

Animals↗
PubMed1976

Operant conditioning of heart rate in free-moving dogs.

The magnitude of changes in heart rate that could be induced by the operant conditioning of beat-to-beat intervals was determined. Shock avoidance methods were employed during 71 sessions conducted over 17 weeks in 3 free-moving mongrel dogs. Experimental periods during which conditioning was done alternated with baseline periods. Heart rate differences between baseline and experimental periods were used as indices of conditioning. Alterations in heart rate were compared among four types of sessions: control, random shock, decrement conditioning and increment conditioning. Conditioned heart rate decrements averaged 3% while heart rate increments averaged 10%. Thus, operant conditioning carried out over prolonged periods of time resulted in relatively minor changes in heart rate.

Animals↗
PubMed1976

Muscarinic effects of vagosympathetic trunk stimulation on the repetitive extrasystole (RE) threshold.

The precise mechanism of the vagus in opposing adrenergic influences on cardiac vulnerability has not been defined. In the present investigation, cholinergic stimulation was produced by administering the selective muscarinic agent methacholine (MCh) and ventricular vulnerability was assessed by measuring the repetitive extrasystole (RE) threshold. MCh produced a sustained 98 +/- 12% (P less than 0.0001) increase in the RE threshold; the increase was abolished by concurrent infusion of atropine (0.2 mg/kg). When MCh was administered during beta-adrenergic blockade with propranolol, however, no further increase in RE threshold occurred beyond that resulting from propranolol alone. Infusion of norepinephrine (NE), in a dose insufficient to provoke systemic hypertension, significantly lowered the vulnerable period threshold. This decrease was completely abolished by concurrent vagosympathetic stimulation (VS). It is concluded that VS affects ventricular vulnerability through its muscarinic action and that the protection against VF is in part due to modulation of neural and humoral beta-adrenergic inputs.

Animals↗
PubMed1975

Programmed "trendscription." A new approach to electrocardiographic monitoring.

A new approach to monitoring of episodic but frequently recurring arrhythmias has been developed, consisting of condensation of electrocardiographic information on a special drum recorder, a programmer that permits selection of intervals and durations for monitoring, and a telemetry unit for transmission of the electrocardiographic signal. We used this system to manage three selected cases.

Adrenergic beta-Antagonists↗
PubMed1975

Comparison of ventricular ectopic activity during 24-hour monitoring and exercise testing in patients with coronary heart disease.

The exposure of ventricular ectopic activity (VEA) by maximal exercise testing and 24-hour ambulatory monitoring was compared in 100 unselected patients with coronary heart disease. The arrhythmia was noted with exercise in 56 patients and with monitoring in 88. Repetitive forms such as couplets and ventricular tachycardia were found to be twice as frequent (40 vs. 20) with monitoring than with exercise. Patients with prior myocardial infarction had more frequent ventricular ectopic activity of a more advanced grade with both exercise and monitoring than patients with angina pectoris. Exercise exposed the grades of ectopic activity that recurred during two or more hours of the monitoring session. Of seven patients with ventricular tachycardia on exercise only four exhibited this grade with monitoring. It may be that these two methods divulge different information regarding the electrophysiologic state of the myocardium.

Adult↗
PubMed1975

Vulnerability to ventricular fibrillation during acute coronary arterial occlusion and release.

The effect of 10 minutes of occlusion, and release of occlusion, of the left anterior descending coronary artery on vulnerability to ventricular fibrillation was studied in 15 dogs. Ventricular fibrillation threshold was determined by inducing a sequence of three closely coupled extrasystoles (sequential R/T pulsing). Within 3 minutes of occlusion the current required to induce fibrillation decreased from a control value of 56 +/- 7 ma (mean +/- standard error) to 1.6 +/- 0.3 ma (P less than 0.001). It remained at this level for about 4 minutes and then rapidly returned to the control level in 8 of 10 dogs. Upon release of occlusion at 10 minutes, the ventricular fibrillation threshold was again greatly reduced; this period of reduction occurred shortly after reperfusion and was of brief duration. After both occlusion and release the duration of the ventricular vulnerable period was prolonged. The time course of change in cardiac vulnerability parallels the altered susceptibility to ventricular fibrillation after coronary arterial occlusion and release. These results recommend sequential R/T pulsing as a useful technique for probing changes in cardiac vulnerability under diverse experimental conditions.

Acute Disease↗
PubMed1975

Effect of posterior hypothalamic stimulation on ventricular fibrillation threshold.

The effect of posterior hypothalamic stimulation on cardiac susceptibility to ventricular fibrillation (VF) was studied in 34 dogs. VF threshold was determined by inducing a sequence of early extrasystoles (R/T pulsing). Hypothalamic stimulation was associated with sinus tachycardia, systemic hypertension, and a 40% reduction in VF threshold. The effects of hypothalamic stimulation on the VF threshold persisted when heart rate acceleration and the pressor response were prevented. Cervical vagotomy and bilateral adrenalectomy were likewise without effect on fibrillation threshold changes. However, the decrease in threshold was abolished by beta-adrenergic blockade. It is concluded that the reduction in VF threshold associated with hypothalamic stimulation derives from the direct action of sympathetic nerves upon the myocardium, rather than from secondary hemodynamic effects.

Adrenal Glands↗
PubMed1975

The effect of vagus nerve stimulation upon vulnerability of the canine ventricle: role of sympathetic-parasympathetic interactions.

The effect of vagus nerve stimulation (VNS) upon ventricular vulnerability was studied in 30 mongrel dogs subjected to varying levels of adrenergic stimulation. Vulnerability was assessed both by determining the minimum current required to produce ventricular fibrillation (VF threshold) and by plotting VF threshold throughout the vulnerable period (VF zone). Chloralose-anesthetized animals were studied by means of sequential pulses applied to the apex of the right ventricular endocardium. Testing was carried out in closed-chest dogs, in open-chest dogs with and without left stellate ganglion stimulation (LSGS), and in open- and closed-chest dogs pretreated with propranolol. In the absence of adrenergic stimulation. VNS was without significant effect on either the VF threshold or the VF zone under closed- or open-chest conditions. During LSGS, however, VNS was associated with a 93 +/- 22% (mean +/- SE) increase in VF threshold (P less than 0.01) and constriction of the VF zone. Vagus nerve stimulation combined with LSGS raised VF threshold to the control value, but not beyond. After beta-adrenergic blockade with propranolol, VNS was without effect on VF threshold in either open- or closed-chest animals. It is concluded that augmented sympathetic tone is a precondition for a VNS-induced elevation in VF threshold. The vagal effect is indirect and is expressed by opposing the effects of heightened adrenergic tone on ventricular vulnerability.

Acetylcholine↗
PubMed1975

Cardioversion 1975: foremost therapy for tachyarrhythmias.

Extensive clinical experience indicates that cardioversion is the most effective method now available for terminating cardiac tachyarrhythmias. This procedure is not accompanied by depression of myocardial contractility, conductivity, or excitability, a common sequel to the use of antiarrhythmic drugs. Furthermore, the incidence of complications with cardioversion is low. These features of effectiveness, safety, and simplicity permit cardioversion to be used by the noncardiologist physician, who may be less experienced than a cardiologist in recognizing arrrhythmias. Cardioversion has not reduced the need for antiarrhythmic agents; on the contrary, more such drugs are required to maintain normal sinus rhythm. The problem at present is not the terminating a tachyarrhythmia but in preventing its recurrence.

Adrenergic beta-Antagonists↗
PubMed1975

Monitoring for serious arrhythmias and high risk of sudden death.

Ventricular premature beats (VPBs) are present in 85% of patients with coronary heart disease (CHD). A classification of VPBs based on frequency, multiformity, repetitive pattern, and degree of prematurity promises to aid in identifying patients at high risk of sudden death. Advanced grade or repetitive forms of VPBs are observed in 41% of patients with CHD who are monitored for 24 hours while ambulatory. Exercise stress is less effective than monitoring, but when advanced grades are exposed by exercise, they are likely to be persistent for two or more hours during monitoring. Such persistent and advanced grades characterize patients with multivessel coronary artery disease. Diurnal variations occur in VPB frequency and pattern with significant reduction during sleep. This as well as other facts suggest a primary role for neural activity in the genesis of ventricular ectopy. The relevance of these observations to sudden death is considered.

Aged↗