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Results for “PRENYLAMINE”

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At least 55 records · Page 3Linked to original sources
PubMed1977

[Studies on the mechanism of action of vascular spasmolytics. 3. Effect of nitroprusside sodium, nitroglycerin, prenylamine and verapamil on the fluoride-induced contracture of the isolated coronary artery].

On isolated coronary arteries of cattle, nitroprusside-sodium, nitroglycerol, prenylamine, and verapamil were studied for their spasmolytic effects on a contracture induced by fluoride ions. With this contracture model, which is independent of extracellular calcium, nitroprosside-sodium and nitroglycerol showed strong spasmolytic action. Verapamil proved ineffective, and the effectiveness of prenylamine was strongly reduced. The results lend support to earlier findings suggesting that nitroglycerol and nitroprusside-sodium are endowed with a relaxation mechanism different from that of verapamil and analogously acting compounds.

Animals↗
PubMed1977

[Experiments on the mechanism of action of vascular spasmolytics. 4. Effect of nitroprusside sodium, nitroglycerin, prenylamine and verapamil on the calcium uptake of microsomes of the smooth bascular muscles].

Nitroprusside-sodium, nitroglycerol, and verapamil had no effect on the calcium uptake by microsomes from the carotid artery of cattle. Prenylamine reduced the passive binding and the active uptake and released already bound calcium. The basal Mg-dependendent ATPase and Ca-stimulatable Mg-ATPase were inhibited by prenylamine.

Animals↗
PubMed1976

[Experments on the mechanism of action of vascular spasmolytic agents. I. Effect nitroprusside sodium, nitroglycerine, prenylamine and verapamil on the arrested potassium contracture of isolated coronary arteries].

On the potassium contracture of isolated coronary arteries of cattle, the relaxation effected by calcium depletion can be blocked by lanthanum ions. The contracture persisting in calcium-free solution (arrested potassium contracture) is used to differentiate the sites of attack of spasmolytics. Verapamil and prenylamine are ineffective in this contracture model. By contrast, nitroprusside sodium and nitroglycerol as before act spasmolytically. Thus, both groups of drugs act through basically different sites. The findings are consistent with the hypothesis that the spasmolytic action of verapamil and prenylamine is based on a blockade of calcium influx. For nitroprusside sodium and nitroglycerol such a mechanism on the arrested potassium contracture has to be ruled out.

Animals↗
PubMed1976

[Experiments on the mechanism of action of vascular spasmolytic agents. II. Action of nitroprusside sodium, nitroglycerin, prenylamine and verapamil on the lanthanum contracture of isolated coronary arteries].

On isolated coronary arteries of cattle, lanthanum causes after preceding calcium depletion by EGTA a contracture which is independent of the presence of extracellular calcium. Nitroprusside sodium and nitroglycerol act on this contracture strongly relaxing in the same concentrations that were active on the potassium contracture. In contrast, a very low spasmolytic effect is demonstrable for verapamil on the lanthanum contracture, and prenylamine is without any statistically significant influence. Nitroprusside sodium and nitroglycerol and act by a mechanism entirely different from that of verapamil and prenylamine.

Animals↗
PubMed1979

Prenylamine. Autoradiographic and neuropathological studies on myocardial mechanisms of action.

Myocardial localization of prenylamine (PNL), a well known antianginal drug, was studied by means of an autoradiographic technique to detect microscopical distribution of tritiated PNL (3H-PLN). Forty Wistar rats received 35 muCi/kg b. w. 3H-PNL i. p., the animals being killed 30 min after injection. Heart slices, 1 mm thick, were processed for both autoradiographic and conventional histological techniques. 3H-PNL was observed, mainly, as striae along sarcolemma; sarcolemmal/intramyocardial 3H-PNL distribution ratio was 6 : 1. Preferential membrane deposition of 3H-PNL is probably related to the calcium transport inhibiting action of the drug, previously described.

Animals↗
PubMed1987

Prevention of adriamycin-induced cardiotoxicity by prenylamine: a pilot double blind study.

Adriamycin (ADM) is an effective antineoplastic drug. However, the amount of ADM that can be administered must be limited because of the risk of developing a severe dose-dependent myocardiopathy. Prenylamine (PNL), a calcium antagonistic drug, provided partial protection against ADM-induced cardiotoxicity in mice and in the rabbit. Thus, it was considered important to evaluate the cardioprotective potential of PNL in patients given ordinary doses of ADM. Twenty-six patients were selected and randomized in two groups, and a double-blind trial was begun. Group A (n = 13): patients received ADM, i.v. at standard oncological doses up to 550 mg/m2, plus placebo, orally. Group B (n = 13): ADM was administered as in Group A, but PNL 200 mg/day was given instead of placebo. Standard ECG and chest radiographs were performed at the beginning of treatment and every two months. Mode-M echocardiograms and 24-hour ambulatory ECGs were obtained previously to the beginning of the ADM treatment and two months after the administration of the last dose of the drug. In Group A, three patients died from oncological causes, total ADM dose was 359 +/- 100 mg/m2, and the mean age was 59.7 years. One patient in this group developed a congestive myocardiopathy while another patient developed a severe supraventricular arrhythmia. In Group B, four patients died from oncological causes, total ADM dose was 367 +/- 132 mg/m2, and the mean age was 63.8 years. No myocardiopathy was found in this group. These findings suggest that simultaneous administration of PNL may mitigate ADM cardiotoxicity, but larger trials are needed to draw definite conclusions.

Aged↗
PubMed1993

Effects of prenylamine and AQ-A 39 on reentrant ventricular arrhythmias induced during the late myocardial infarction period in conscious dogs.

The effects of prenylamine (PNL) and AQ-A 39 on sustained ventricular tachycardia (SVT) were studied by programmed stimulation in conscious dogs 4-10 days after ligation of the left anterior descending (LAD) coronary artery. In 8 of 16 dogs developing SVT in the control, PNL (3 mg/kg intravenously, i.v.) suppressed inducibility of SVT and slowed the rate of tachycardia in 6 other animals. In a separate group of 10 dogs with inducible SVT, AQ-A 39 (4 mg/kg i.v.) abolished elicitation of tachycardia in 3 dogs and decreased its rate in 6 other dogs. Neither drug affected normal conduction significantly, but PNL impaired slow conduction in the infarct zone, as indicated by prolongation of late potential. Both agents increased the effective refractory period (ERP) of infarcted and normal ventricular myocardium and prolonged the corrected QT interval. PNL and AQ-A 39 exert notable efficacy in preventing infarcted heart from severe ventricular arrhythmias. Prolongation of ventricular refractoriness and repolarization, as well as decreased slow conduction in ischemically damaged myocardium, are major mechanisms accounting for the effectiveness of these drugs against ventricular arrhythmias.

Animals↗
PubMed1980

The effect of prenylamine on the QT interval of the resting electrocardiogram in patients with angina pectoris.

Resting ECGs were recorded in 29 patients with angina pectoris before, during and after treatment with prenylamine 180 mg daily. The QT interval became significantly prolonged after one week of treatment. The prolongation persisted as long as therapy was continued, which was up to 6 months. After withdrawal of treatment the QT interval returned to normal within 2 weeks. In this study no serious problems were encountered by those patients in whom the QT interval was prolonged.

Adult↗
PubMed1981

A case of prenylamine toxicity showing the torsade de pointes phenomenon in sinus rhythm?

A case of torsade de pointes attributed to prenylamine is described. In addition, the authors show QRS axis variation of a similar nature in sinus rhythm. It is postulated that these changes of QRS axis direction, seen in ventricular tachycardia and sinus rhythm, are both manifestations of partial refractoriness, within the ventricle, producing gross changes in the mean QRS vector.

Electrocardiography↗
PubMed1982

An overall review on prenylamine mechanisms of action in experimental models of myocardial damage.

In this review we present the effects of a well-known antianginal drug, prenylamine (PNL), in experimental models of acute myocardial damage induced by a beta-agonistic drug, isoproterenol (ISP), in several trials conducted in our laboratory in both rats (n = 204) and monkeys (n = 26). PNL significantly inhibited ISP-induced lesions, protecting the majority of animals studied. Studies dealing with the site of action of the drug, such as 45Ca, 3H-PNL and 3H-ISP trials, showed a clear membrane effect slowing down Ca transport. Correlation between ECG (inhibition of ST depression after ISP) and pathological findings in monkeys was also obtained in one of our experiments. These series of assays were useful in obtaining a more complete idea of activity and site of action of the drug. It seems that, in acute models, PNL acts as a calcium antagonistic drug rather than an adrenergic moderator.

Angina Pectoris↗
PubMed1976

[The effect of oxyfedrine, prenylamine and dipyridamole on heart hypertrophy and collagen concentration of pressure loaded rat hearts].

Rats were subjected to constriction of the abdominal aorta and two days later to nephrectomy. The maximum left ventricular hypertrophy was reached on the seventh day following the nephrectomy. During one month the animals were treated, six days per week with i.p. dipyridamole, prenylamine or oxyphedrine. The drugs studied suppressed the increase in hydroxyproline concentration of the left ventricle whereas the development of heart hypertrophy was not influenced.

Animals↗
PubMed1985

Prenylamine inhibition of adriamycin-induced myocardiopathy.

Adriamycin (ADM) is an effective antineoplastic drug. However, ADM induces alterations in cardiac function which limit the safe dose which can be administered. As it was suggested that ADM-induced cardiomyopathy is related to a calcium mediated necrosis and/or an increase in lipid peroxidation, the cardioprotective potential of prenylamine (PNL) (a well known calcium antagonistic drug) was evaluated in rabbits given chronically large doses of ADM. Twenty five rabbits were allotted to 4 groups. Group I (PNL-ADM) was given 334 +/- 82 mg of PNL and 12.2 +/- 3.8 mg of ADM, group II (water-ADM) 14.4 +/- 4.6 of ADM, group III (PNL-saline) 280 +/- 91 mg of PNL and group IV (water-saline), same doses as ADM and PNL. Rabbits were sacrificed between 38 and 65 days after the beginning of the trial. In group I weight increased only 13% and in group II, 39% (p less than 0.01). Correlation coefficients were significant for variations of weight and ADM-doses (r = 0.875). In group II 8/10 rabbits showed post-treatment electrocardiographic changes, while group I changes were found in a lesser extent (5/10). Heart homogenates from ADM-treated rabbits showed an increased lipoperoxidation (74 +/- 5 cpm/mg protein X 10(-3) as compared with the control animals (58 +/- 6 cpm/mg protein X 10(-3) (p less than 0.05), while PNL treatment did not alter myocardial lipoperoxidation. Microscopically, myocardial fibers had from mild to severe hydropic vacuolization of sarcoplasm which led to progressive myocytolysis. Myocardial damage was lower in group I (ADM-PNL), 41.7 +/- 7.6 than in group II (water-ADM), 104 +/- 10.8 (p less than 0.05). It is suggested that ADM-peroxidation effects lead to lipoperoxidation with membrane damage and increase in Ca++ permeability, the latter being counteracted by PNL.

Animals↗
PubMed1976

[Adverse effects of drugs: syncope due to prenylamine (author's transl)].

The authors report on 4 Intensive Care Unit cases, hospitalized for syncopes due to serious ventricular arrhythmias. They all presented long Q-T and were receiving treatment with prenylamine. Improvements were observed on suspension of the drug, suggesting therefore that during this treatment, frequent electrocardiographic checks, especially for elderly patients, should be carried out. Caution should also be exercised in associations with other chinidinosimiles and hypokaliemic drugs

Aged↗