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Biomedical subjects

B Lown

Publications and source records attributed to B Lown.

At least 181 records · Page 10Linked to original sources
PubMed1978

Roles of psychologic stress and autonomic nervous system changes in provocation of ventricular premature complexes.

Neural and psychologic factors have been implicated as risk factors for ventricular arrhythmias and sudden death in man. However, the relation between these factors and arrhythmia has hitherto not been systematically explored. We examined the effect of psychologic stress testing in 19 patients with advanced grades of ventricular arrhythmias. Psychologic stress consisted of mental arithmetic, reading from colored cards and recounting emotionally charged experiences. Such testing induced a significant increase in ventricular premature beat frequency in 11 of 19 patients (P less than 0.05). One patient experienced paroxysms of ventricular tachycardia. In 14 of these 19 patients elicitation of vagal or sympathetic autonomic reflexes failed to induce significant arrhythmia in all but one patient. It is concluded that (1) objective psychologic tests may precipitate ventricular arrhythmia in susceptible patients, and (2) evocation of peripheral autonomic reflexes is an insufficient trigger for enhanced ventricular ectopic activity.

Adolescent↗
PubMed1978

Effects of clonidine on vulnerability to fibrillation in the normal and ischemic canine ventricle.

Clonidine infusion (10 microgram/kg, i.v.) elicited a 30% increase in repetitive extrasystole (RE) threshold in 6 chloralose-anesthetized dogs. A reduction in heart rate and arterial blood pressure accompanied the increased threshold. Intracisternal injection of clonidine (2 microgram/kg) in 6 dogs caused similar alterations in these parameters. Bilateral vagotomy, performed in 6 dogs prior to intravenous clonidine, prevented the increase in RE threshold but did not prevent the drug-induced bradycardia. Atropine (0.2 and 0.6 mg/kg), however, did not attenuate the effect of clonidine on RE threshold. Clonidine administration did not prevent the reduction in ventricular fibrillation threshold associated with a 10 min occlusion of the left anterior descending coronary artery or following reperfusion. We conclude that: (1) clonidine reduces ventricular vulnerability in the normal but not the ischemic heart, and (2) its protective effect is mediated by enhanced afferent vagal input to midbrain cardiovascular regulatory centers. This central nervous system action causes a reduction in sympathetic tone to the heart.

Animals↗
PubMed1978

The effects of psychological stress and vagal stimulation with morphine on vulnerability to ventricular fibrillation (VF) in the conscious dog.

Ventricular vulnerability to fibrillation was assessed in 12 conscious dogs in aversive and nonaversive environments using the repetitive extrasystole (RE) threshold method. In the average environment, RE threshold was 45 per cent lower than in the nonaversive setting and heart rate and blood pressure were significantly elevated. This decrease in RE threshold occurred within 10 minutes of exposing the animals to stress. In contrast, the recovery in RE threshold in the nonaversive setting occurred over a 40 minute period. When morphine sulfate (MS) 0.25 mg./Kg was administered to dogs in the aversive environment, the RE threshold was significantly increased. Cholinergic blockade of vagal efferent activity with atropine (0.2 mg./Kg) annulled partially the effect of MS on RE threshold MS was without effect in the nonaversive environment. It is concluded that MS exerts a significant protective effect on increased ventricular vulnerability associated with psychological stress. This effect is mediated by the vagotonic and sedative actions of morphine.

Animals↗
PubMed1978

Central neurochemical factors related to serotonin metabolism and cardiac ventricular vulnerability for repetitive electrical activity.

Sympathetic neural activity modifies cardiac excitability and lowers the threshold of the vulnerable period for ventricular fibrillation. Sympathetic neural traffic to the heart can be diminished by administering serotonin precursors that localize in the central nervous system. In this study anesthetized dogs were injected with either of the serotonin precursors L-tryptophan or 5-hydroxy-L-tryptophan in conjunction with the monoamine oxidase inhibitor pheneizine and the selective peripheral L-amino acid decarboxylase inhibitor carbidopa. Ventricular vulnerability was evaluated by measuring the repetitive extrasystole threshold. A sustained increase of 50 percent in this threshold resulted only with use of biochemical measures that presumably increase serotonin levels in the central nervous system. Thus neuropharmacologic measures affecting central sympathetic activity alter cardiac vulnerability and may protect against ventricular fibrillation.

5-Hydroxytryptophan↗
PubMed1978

Precordial mechanical stimulation for exposing electrical instability in the ischemic heart.

Sequenital mechanical pulsing of the chest wall with three stimuli failed to induce arrhythmias in normal dogs. After coronary arterial occlusion, this technique evoked in 11 of 12 animals repetitive ventricular tachycardia in 2. These responses corresponded closely to those elicited by electrical testing. In four conscious animals after recovery from myocardial infarction, precordial pulsing induced repetitive ventricular arrhythmias. The type of arrhythmia produced depended on the degree of prematurity of the third pulse in the sequence. The use of precordial mechanical stimulation can perhaps be modified and adapted as a method of detecting persons at high risk for sudden cardiac death.

Animals↗
PubMed1978

Protective effect of the vagotonic action of morphine sulphate on ventricular vulnerability.

Administration of morphine sulphate to 16 anaesthetised dogs resulted in significant reduction in ventricular vulnerability to fibrillation. The repetitive extrasystole threshold was used as an index of vulnerability to ventricular fibrillation. In 14 dogs, atropine or vagotomy abolished this response. This suggests that central vagal activation by morphine sulphate may be protective against ventricular fibrillation.

Animals↗
PubMed1978

Energy requirement for defibrillation of a markedly overweight patient.

Recommendations have been made recently that the energy output of present-day defibrillators be increased above the 400 wsec limit. These recommendations are based largely on experimental studies in animals. We report a case of a man weighing 190.1 kg (418.2 lb), successfully resuscitated with a single 400 wsec shock after a prolonged episode of ventricular fibrillation. The observation in this patient as well as data derived from cardiovascular experience indicates that weight is not a significant factor in the successful outcome following defibrillation in adults. Many variables primarily related to the clinical condition of the heart influence the results of countershock. There are no valid studies at present to support the claim that high-energy defibrillators are necessary. In fact, implementation of such a recommendation is premature and possibly dangerous.

Adult↗