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Results for “Bretylium Compounds”

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PubMedDate not supplied

[Action of ornid and papavperine on the biopotential and electrolytic balance of the vascular wall].

The influence of ornidium (bretylan) and papaverine on the biopotential and electrolytes metabolism in the vascular wall was studied in tests with cats. With their single administration ornidium (30 mg/kg) and papaverine (10 mg/kg) were found to increase the electrongegative biopotential and the potassium content in the vasculr wall. Ornidum causes the amount of magnesium to augment in the wall of venous vessels and of calcium--in the abdominal aorta. When used course-wise papaverine dose not produce any changes in the biopotential, but increases the potassium content in the venous vessels and decreases the amount of magnesium in the abdominal aorta.

Animals↗
PubMed1977

[Antiarrhythmic activity of adrenergic blockaders with different mechanisms of action].

Experiments have demonstrated that Alfeprol arrests atrial fibrillation in dogs induced by electric stimulation of the heart, and atrial fibrillation in cats modelled by Akonitine application; it suppresses ventricular tachycardia in dogs occurring following an occlusion of the branches of coronary arteries, and in cats when induced by strophantin intoxication; it prevents fatal ventricular fibrillation in rats poisoned by calcium chloride. The antiarrhythmic effect of Anaprille was not so persistent and manifested itself only in cases of some particular rhythm disorders. Ornid displayed no antiarrhythmic activity. The blocking of adrenergic innervation of the heart by means of beta-adrenergic blockers (Alfeprol, Anaprilline) and sympatholytic (Reserpine, Ornid) considerably increased the animals tolerance of the toxic effect of strophantin, decreasing its arrhythmogenic effect in particular. The mechanisms of the antiarrhythmic effect of antiadrenergic agents are discussed along with the possibilities of their employment for the correction of cardiac sensitivity of glycosides.

Alprenolol↗
PubMedDate not supplied

Experimental and clinical pharmacology of bretylium tosylate in acute myocardial infarction: a 15-year journey.

Experimental and clinical studies demonstrate the antifibrillatory effectiveness of bretylium tosylate: Experimental ventricular fibrillation induced either by electrical stimulation or by ischemia is prevented by bretylium. In 2,000 acute myocardial infarction patients who received bretylium prophylactically primary ventricular fibrillation occurred in less than 1% of cases. In a randomized hemodynamic study in acute myocardial infarction patients bretylium induced a significant decrease in heart rate, systolic and mean left ventricular pressures, and in systolic and mean aortic pressures. In addition, a parallel and significant decrease in total pulmonary and systemic resistances was seen, accompanied by decreases in tension time and left ventricular (delta P/delta V) indexes. Bretylium tosylate induces stabilization of electrical systole duration (QTc) in acute myocardial infarction patients. The conclusions of the present review strongly support those of the United States Food and Drug Administration, approving bretylium for prophylaxis and treatment of ventricular fibrillation.

Animals↗
PubMed1979

Bretylium tosylate: a review.

The chemistry, pharmacology, pharmacokinetics, clinical uses, adverse effects, drug interactions and dosage of bretylium tosylate, a recently approved antiarrhythmic agent, are reviewed. Bretylium tosylate is used to treat life-threatening ventricular arrhythmias, principally ventricular fibrillation and ventricular tachycardia, that have not responded to treatment with first-line antiarrhythmic agents. The drug has a direct positive inotropic effect on the myocardium and blocking effect on postganglionic sympathetic nerve transmission. The drug is poorly absorbed orally, requiring either i.m. or i.v. administration. Drug excretion occurs primarily through the kidney, necessitating dosage modification in renal disease. Hypotension is the most commonly observed adverse reaction to bretylium tosylate. Rapid i.v. administration may cause severe nausea and vomiting, and i.m. injection at the same site may cause atrophy and necrosis of muscle tissue. Quinidine and procainamide may potentiate the hypotensive effects of bretylium. Bretylium will aggravate digitalis-induced arrhythmias. Bretylium's use in resistant ventricular tachyarrhythmias requires close clinical monitoring.

Arrhythmias, Cardiac↗
PubMed1985

Muscarinic receptor heterogeneity revealed by interaction with bretylium tosylate. Different ligand-receptor conformations versus different receptor subclasses.

The interaction of the antiarrhythmic drug, bretylium tosylate, with the muscarinic receptor in tissue homogenates from regions of rat brain and heart and from submandibular gland and ileal wall was investigated. Competition binding experiments were carried out using the highly specific tritiated antagonist N-methyl-4-piperidyl benzilate. Bretylium displayed heterogeneous binding characteristics. The binding of the drug to neural and glandular preparations was found to be best fitted by a one-site model in each case. On the other hand, in the case of muscle preparations (heart and ileum), a two-site model yielded a significantly better fit for the binding data than that given by a single site model. High affinity sites for the drug were detected in the muscle tissue only, with equilibrium binding constants of 0.24 +/- 0.12, 0.97 +/- 0.27, and 0.57 +/- 0.41 microM for the atrium, ventricle, and ileum, respectively. The low affinity binding constants in the muscle tissues were similar (approximately 10 microM) to those in the neural and glandular tissues examined, namely, the cortex, the hippocampus, the medulla pons, and the submandibular gland. The drug had no effect on agonist-binding characteristics. The heterogeneous binding of bretylium is compared to that of another nonclassical antagonist, pirenzepine. The results are discussed in relation to two alternative hypotheses put forward to account for antagonist heterogeneity in binding, the one involving ligand-receptor conformations and the other receptor subclasses.

Animals↗
PubMed1985

[Neurochemical mechanisms of artifical hypobiosis and chemical thermoregulation].

Artificial hypobiosis in rats and rabbits was modelled using ornid which caused the blockade of neurotransmitter release from adrenergic neurons. The data obtained corroborated the hypothesis of the mechanisms of chemical thermoregulation as well as new ways of controlling these processes up to their complete blockade by means of decreasing adrenergic effects in the organism. Warm-blooded animals were transferred into poikilothermic state and then into hypobiosis under any given body temperature. At 18-20 degrees C, metabolism may be decreased to 1/10 of standard values and the state of hypobiosis may be maintained for a prolonged period remaining eversible without application of any drugs activating or blocking physiological functions.

Adrenergic Fibers↗