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S H Rabinowitz

Publications and source records attributed to S H Rabinowitz.

9 recordsLinked to original sources
PubMed1998

Prodrug ACE inhibitors.

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Angiotensin-Converting Enzyme Inhibitors↗
PubMed1979

Central serotonergic agents raise the repetitive extrasystole threshold of the vulnerable period of the canine ventricular myocardium.

Systemic administration of three central serotonergic agents, melatonin, 5-methoxytryptophol, and 6-chloro-2-(1-piperazinyl)-pyrazine (MK-212), produced significant increases in the threshold of the vulnerable period for repetitive electrical activity in the canine cardiac ventricle. MK-212 was effective despite bilateral vagotomy. The specific serotonin antagonist, metergoline, blocked the effect of MK-212 on the threshold. An increase in central serotonergic activity may inhibit the flow of arrhythmogenic sympathetic nerve traffic from the brain to the heart.

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↗
PubMed1977

Neural and psychologic mechanisms and the problem of sudden cardiac death.

Brain stimulation can provoke a variety of arrhythmias and lower the ventricular vulnerable threshold. In the animal with acute myocardial ischemia such stimuli suffice to provoke ventricular fibrillation. Vagal neural traffic or adrenal catecholamines are not the conduits for this brain-heart linkage. Accompanying increases in heart rate or blood pressure are not prerequisites for the changes in cardiac excitability. Increased sympathetic activity, whether induced by neural or neurohumoral action, predisposes the heart to ventricular fibrillation. Protection can be achieved with surgical and pharmacologic denervation or reflex reduction in sympathetic tone. With acute myocardial ischemia, augmented sympathetic activity accounts for the early surge of ectopic activity frequently precipitating ventricular fibrillation. Asymmetries in sympathetic neural discharge may also contribute to the genesis of serious arrhythmias. The vagus nerve, through its muscarinic action, exerts an indirect effect on cardiac vulnerability, the consequence of annulment of concomitant adrenergic influence, rather than of any direct cholinergic action on the ventricles. There exist anatomic, physiologic as well as molecular bases for such interactions. Available experimental evidence indicates that environmental stresses of diverse types can injure the heart, lower the threshold of cardiac vulnerability to ventricular fibrillation and, in the animal with coronary occlusion, provoke potentially malignant ventricular arrhythmias. Available evidence indicates that in man, as in the experimental animal, administration of catecholamines can induce ventricular arrhythmia, whereas vagal activity exerts an opposite effect. Furthermore, in certain subjects diverse stresses and various psychologic states provoke ventricular ectopic activity.

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↗