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733 records · Page 41Linked to original sources
PubMed1982

Increased accumulation of vincristine and adriamycin in drug-resistant P388 tumor cells following incubation with calcium antagonists and calmodulin inhibitors.

Some calcium antagonists and calmodulin inhibitors enhance the intracellular levels of vincristine and Adriamycin in vincristine- and Adriamycin-resistant P388 leukemia cells by inhibiting their outward transport. The high intracellular drug accumulation was directly related to the enhancement of the cytotoxicity of the antitumor agents, and the vincristine and Adriamycin resistance in these cells was circumvented.

Animals↗
PubMed1980

[Effect of odiphalin and difril on catecholamine concentration in adrenergic nerve fibers of different rat organs].

The histochemical method of Axelsson coupled with photometry was used to study variations in the content of biogenic amines in different rat organs (myocardium, vas deferens, mesenteric vessels, iris, atrial and ventricular heart valve) under the effect of odiphalin and difril. The results obtained indicate that the organs with direct, indirect and mixed innervation differ in the pattern of response to the pharmacological agents administered. Venous vessels proved to be the most sensitive to the action of odiphalin and difril. The data obtained warrant a conclusion about the heterogeneity of adrenergic nerves in organs and tissues.

Adrenergic Fibers↗
PubMed1978

["Torsades de pointe" and reentry induced by anti-arrhythmia agents].

Some anti-arrhythmic agents which have a stabilising effect on the membrane, particularly those belonging to Group I of Vaughan William's classification, are likely to cause rythmic disturbances by a re-entry phenomenon (atrial flutter 1/1, premature ventricular contractions, ventricular tachycardia, "torsades de pointe", even fatal ventricular fibrillation). The quinidines have been the most often condemned due to their effect on the action potential and on the speed of conduction. The fact that these re-entry phenomena are more frequent at therapeutic doses than at high or toxic doses suggests an individual susceptibility and the interaction of various predisposing factors: renal insufficiency, potassium depletion, pre-existing conduction disturbances, potentialsing drugs. In order to prevent these incidents it is advisable not to prescribe such anti-arrhythmic agents for susceptible patients, to control individual tolerance and to watch for the first ECG signs of conduction disturbances or of re-entry, such as premature contraction with fixed coupling. Treatment consists in an electrosystolic stimulus and the possible administration of potassium and bretylium.

Adrenergic beta-Antagonists↗
PubMed1976

[Longterm treatment of coronary heart disease with Segontin (author's transl)].

62 patients with coronary heart disease were treated with Segontin 60 mg for periods of 6 months to 8 years in a specialist internal medical practice. The average maintenance dose was 2 Segontin 60 mg dragees daily. Segontin 60 was distinguished by a high success rate under practice conditions with good tolerance at the same time. Because of its additional sympathicolytic antiarrhythmic and central sedative action, Segontin 60 is a particularly valuable preparation of the calcium antagonist series with which it also shares the circulation-promoting and coronary analge sic actions and economizing effect on the heart metabolism. It has proved itself very good for the treatment of angina pectoris conditions in patients with coronary heart disease. Moreover, Segontin 60 mg is the preparation of choice if the coronary heart disease is accompanied by tachyarrhythmic and hyperkinetic symptoms.

Angina Pectoris↗