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At least 19 recordsLinked to original sources
PubMed1981

[The action of oxyfedrine on haemodynamics, inotropism and blood perfusion of the partially ischaemic myocardium after digoxin premedication. Studies on anaesthetized dogs (author's transl)].

The effect exerted on the partially ischaemic heart when administering 0.9 mg/kg L-3-(beta-hydroxy-alpha-methylphenethylamino)-3'-methoxypropiophenone (oxyfedrine, ildamen) approx. 10 min after i.v. application of 0.05 mg/kg digoxin was tested on 20 dogs previously anaesthetized with propiomazine-pentobarbital. The following parameters were studied and subsequently compound with the results of former trials of ours' without digoxin premedication: aortic pressure (ASP, ADP), left-ventricular pressure (LVSP, LVEDP), heart rate (HR), cardiac output (HMV), stroke volume (SV), dp/dtmax, dp/dtmax/IP, t-dp/dtmax, blood flow in the normal and partially ischaemic myocardium, the latter being measured with heat conductance probes and labelled microspheres. ASP and ADP show the same reduction--as compared with the control value--both after the administration of oxyfedrine with and without digoxin premedication. After digoxin premedication oxyfedrine led to a somewhat less marked reduction of LVSP; on premedication with digoxin LVEDP was slightly increased whereas it was reduced after additional administration of oxyfedrine as was also the case without digoxin pretreatment. The increase in HR after oxyfedrine is almost the same as without digoxin pretreatment. Also the increase in HMV and the SV lowering are not influenced by digoxin. By administration of oxyfedrine dp/dtmax is always increased by the same amount, starting from the already increased value after digoxin premedication, which is probably an additive effect. The same applies to the quotient dp/dtmax/IP. After oxyfedrine the time t-dp/dtmax is lowered by the same amount, irrespective of a digoxin premedication. Oxyfedrine does not produce a further increase in the heat conductance values after previous application of digoxin; when measuring the blood flow with labelled microspheres the same result was found, which means that by previous administration of digoxin the circulatory effect of oxyfedrine is obviously inhibited. Summing up one can say that by combining the active principles digoxin and oxyfedrine the function parameters of the heart can be influenced only positively.

Anesthesia↗
PubMed1995

Relative bioavailability of DL-oxyfedrine HCl after single-dose oral administration of tablets as compared to equimolar solutions.

The pharmacokinetics and comparative bioavailability of oxyfedrine after single-dose oral administration of oxyfedrine*HCl tablets in comparison to an equimolar aqueous solution of oxyfedrine*HCl were investigated in 12 healthy male subjects. Six of them received 96 mg DL-oxyfedrine*HCl as tablets and solution and the remaining 6 subjects received 16 mg DL-oxyfedrine*HCl as tablets and solution in a randomized cross-over design. For evaluation of the relative bioavailability of the tablet formulation, the main metabolite norephedrine (expressed as hydrochloride) was analyzed in plasma for all 12 subjects. Furthermore, for determination of the parent drug, samples of whole blood were analyzed for DL-oxyfedrine*HCl. Relevant concentrations of the parent drug were found only in the high dosage group. There was no evidence of dose-linearity referring to AUC and Cmax of norephedrine between 16-mg and 96-mg doses of DL-oxyfedrine*HCl. The relative bioavailability of the tablet formulation after administration of 16 mg DL-oxyfedrine*HCl, based on the metabolite norephedrine*HCl was for AUC: 85.37% within a 90% confidence interval of 69.29-105.17% and for Cmax: 78.79% within a 90% confidence interval of 59.19-104.90%. The figures for the 96 mg dose strength were: AUC: 107.85% (90.06-129.15%) and for Cmax: 74.74% (62.48-89.42%).

Administration, Oral↗
PubMed1973

Effects of oxyfedrine on isolated portal vein and other smooth muscles.

1. Oxyfedrine (0.01-1.0 mug/ml), inhibited spontaneous myogenic activity in rat isolated portal vein and carbachol-induced contractions of rat isolated uterus, and relaxed the rabbit duodenum and the guinea-pig tracheal chain preparation. These actions were prevented by the beta-adrenoceptor blocking drug alprenolol. Oxyfedrine was a relatively weak beta-adrenoceptor stimulant (10-100 times less active than isoprenaline) but its actions were more prolonged.2. In the same concentrations, oxyfedrine reduced or prevented the inhibition of myogenic activity of the rat portal vein induced by isoprenaline and by repeated doses of oxyfedrine itself, acting as a partial agonist at beta-adrenoceptor sites.3. Oxyfedrine, 1-12 mug/ml increased myogenic activity in the rat portal vein. This effect was not due to direct or indirect stimulation of alpha-adrenoceptors (because it was unaffected by phentolamine) or to potentiation of acetylcholine or 5-hydroxytryptamine.4. Oxyfedrine (>20 mug/ml) inhibited spontaneous myogenic activity in the portal vein and relaxed the saphenous vein contracted with noradrenaline. This spasmolytic effect of the drug was not due to beta-adrenoceptor stimulation or to inhibition of phosphodiesterase since it was unaffected by alprenolol and by concentrations of imidazole which antagonized the effects of the active phosphodiesterase inhibitor, papaverine. In the portal vein this effect of oxyfedrine was similar to that of the calcium inhibitor iproveratril; some of the effects of oxyfedrine on venous smooth muscle may be mediated through effects on calcium transport.

Adrenergic beta-Agonists↗
PubMed1975

Excretion of norephedrine by man after oral administration of oxyfedrine.

After oral administration of oxyfedrine to healthy volunteers, norephedrine was identified in the urine by thin layer chromatography and gas liquid chromatography and mass spectrography. 30 hours after single oral doses of 8, 16 or 24 mg of oxyfedrine, about 4, 8 and 9 mg, respectively, of norephedrine were found in the urine, i.e. on a molar base 75-100% of the dose was excreted as norephedrine. The peak of excretion occurred within 2-4 hours after administration of the drug. No accumulation of oxyfedrine and/or its metabolite was observed after administration of 16 mg of oxyfedrine t.i.d. for three days. It could not be decided whether oxyfedrine was metabolized to norephedrine by liver enzymes, as in rats, or was spontaneously degraded to norephedrine, e.g. in duodenal fluid before absorption. 30-150 min after oral oxyfedrine (24 mg) norephedrine was demonstrable in duodenal fluid. Thus, in addition to the direct beta-sympathomimetic effects of oxyfedrine, it may also have indirect sympathomimetic effects because of the noradrenaline-releasing properties of its metabolite norephedrine.

Administration, Oral↗
PubMed1978

Effects of oxyfedrin: a beta-adrenoreceptor stimulant, on infarct size following acute coronary artery ligation.

Regional left ventricular blood flow and the extent of myocardial ischaemia were studied after acute coronary artery occlusion in open-chest dogs before and after infusion of oxyfedrin, a beta-adrenergic stimulant. Regional blood flow was measured with radioactive tracer microspheres and local tissue injury was estimated by the S-T segment elevation in epicardial electrocardiograms. Animals receiving oxyfedrin were divided into two groups: 1 and 2. Oxyfedrin was infused intravenously in a dose of 0.80 to 0.94 mg.kg-1 in dogs of group 1 and 1.45 to 1.60 mg.kg-1 in dogs of group 2. The rate of infusion in the animals of both groups was 0.61 mg.min-1. Oxyfedrin caused further S-T segment elevation over ischaemic myocardium and increased the extent of ischaemic injury in group 1 dogs. Conversely, in this same group of dogs, the blood flow was unchanged in low flow regions ( less than 0.3 cm3.g-1.min-1) and increased in higher flow areas, inside the ischaemic region. In the animals of group 2, oxyfedrin caused further S-T segment elevation over ischaemic myocardium and increased the extent of ischaemic injury. Concomitantly, blood flow was significantly reduced both inside and outside the ischaemic region. These observations in dogs of group 1 (ie increased blood flow inside the ischaemic region by infusion of oxyfedrin, in flow zones higher than 0.3 cm3.g-1.min-1, with a further S-T segment elevation over ischaemic myocardium, and an increase in the extent of ischaemic injury) may be explained by a primary effect of oxyfedrin on oxygen demands with secondary changes in blood flow.

Animals↗
PubMed1984

[Mechanism of action of oxyfedrine as a partial beta receptor agonist].

To investigate a possible dual action of oxyfedrine on beta-adrenergic receptors, hemodynamics and systolic time intervals were studied in 12 healthy volunteers during intravenous infusion of isoprenaline. The dose was titrated to a mean target heart rate of 113 bpm corresponding to an average dose of 6.16 micrograms/min. After return to baseline hemodynamics, oxyfedrine was administered as an intravenous bolus of 8 mg and the protocol was repeated. Compared to baseline, the percentage changes induced by isoprenaline at doses of 2.73 and 6.16 micrograms/min before and after (in parentheses) oxyfedrine were: heart rate: +33/+83% (+19/+62%); cardiac output: +90/153% (+30/+71%); systolic blood pressure: +16/+20% (+6/+7%); stroke volume: +42/+38% (+10/+6%); peripheral vascular resistance: -50/-63% (-31/-50%); cardiac work: +86/+148% (+19/+54%); pre-ejection period: -40/-56% (-27/-45%); isovolumic contraction time: -56/-79% (-29/-63%); systolic ejection rate: +67/+103% (+27/+52%); tension time index: +32/+50% (+7/+20%). Thus, the dose-dependent hemodynamic effects of isoprenaline were significantly attenuated by oxyfedrine pre-treatment with a shift of the dose-response curve to the right; this was attributed to a beta-antagonistic property of oxyfedrine. The results indicate that, in view of its well-known beta-stimulating effects, oxyfedrine exerts a dual action on adrenergic beta-receptors consistent with partial agonistic activity. Thereby, the different profiles of hemodynamic and metabolic actions of oxyfedrine compared to those of pure beta-agonistic agents can be explained as well as its beneficial therapeutic effects in patients with coronary heart disease.

Adolescent↗
PubMed1974

The haemodynamic effects of prolonged oral administration of oxyfedrine, a partial agonist at beta-adrenoceptors: comparison with propranolol.

1 Haemodynamic changes have been studied in cats after the chronic oral administration of oxyfedrine (14 mg/kg for 3-4 weeks) or of placebo (lactose). The initial part of the study was carried out under double-blind conditions. The arterial blood pressure was between 19 mmHg (diastolic) and 27 mmHg (systolic) higher in the oxyfedrine treated animals, but there were no differences between the two groups with regard to cardiac output, left ventricular dP/dt max, heart rate or systolic ejection time.2 In cats similarly treated with propranolol (4 mg/kg) there was a slight (12%), but significant, reduction in cardiac output.3 Isoprenaline dose-response curves were shifted to the right in the cats administered oxyfedrine as well as in those administered propranolol. The degree of shift was five-fold (positive chronotropic response) and 20-fold (decrease in diastolic blood pressure) in the oxyfedrine group and 10- and 80-fold, respectively, in the propranolol group.4 In contrast to the partial blockade of the effects of isoprenaline, the haemodynamic response to oxyfedrine was largely unaltered, both in the cats pretreated with propranolol and in those pretreated with oxyfedrine. The pressor response to noradrenaline was potentiated in the cats pretreated with oxyfedrine.5 These results provide an explanation for the anti-anginal action of oxyfedrine. Some degree of beta-adrenoceptor blockade is achieved without a reduction in cardiac output or left ventricular dP/dt max. The relevance of these findings to the haemodynamic situation in angina is discussed.

Administration, Oral↗
PubMed1991

Effects of oxyfedrine on regional myocardial blood flow in patients with coronary artery disease.

Medical treatment of angina pectoris is largely based on the use of beta-blocking agents, calcium antagonists, and nitrates. Oxyfedrine, an amino ketone derivative and partial agonist at beta receptors, has been shown to have potent antianginal properties and to increase coronary blood flow in normal and ischemic myocardial regions in experimental studies. We assessed the effects of intravenous oxyfedrine on regional myocardial blood flow, using positron emission tomography (15-oxygen water), in six patients with chronic stable angina, positive exercise tests, and documented coronary artery disease. Myocardial blood flow was measured in all patients before (baseline) and 10 minutes after the intravenous administration of a single bolus (0.11-0.13 mg/kg) of oxyfedrine. Compared to baseline, heart rate and systolic blood pressure remained almost unchanged after the administration of oxyfedrine. Mean baseline myocardial blood flow was 0.90 +/- 0.15 ml/g/min in areas supplied by arteries with significant coronary stenosis and 1.08 +/- 0.19 ml/g/min in areas supplied by nonstenotic coronary vessels (p less than 0.05). After the administration of oxyfedrine, myocardial blood flow increased significantly in both the regions supplied by stenotic vessels (by 25%; from 0.90 +/- 0.15 to 1.20 +/- 0.31 ml/g/min; p = 0.002) and in areas supplied by angiographically normal coronary vessels (by 22%; from 1.08 +/- 0.19 to 1.38 +/- 0.49 ml/g/min; p less than 0.05). The results of this study indicate that in patients with coronary artery disease, intravenous oxyfedrine significantly increases regional myocardial blood flow, both in areas supplied by critically obstructed vessels and in areas supplied by normal or less severely narrowed coronary arteries.

Aged↗
PubMedDate not supplied

Effect of intravenous oxyfedrine on exercise in patients with ischaemic heart disease.

In a double blind crossover trial, acute effects of 8 mg intravenous oxyfedrine were compared with those of placebo in 18 patients with stable effort angina assessed by treadmill exercise testing. In the resting state, oxyfedrine caused an increase in heart rate (84 +/- 23 to 103 +/- 19 bpm, p less than 0.01), systolic blood pressure (123 +/- 16 to 133 +/- 20 mmHg, p less than 0.01) and double product (11 x 10(3) +/- 2 x 10(3) to 13.7 x 10(3) +/- 3.1 x 10(3), p less than 0.01) as compared to placebo. However, these parameters were not significantly different at the end of first or second stage of the treadmill test (p = NS). Time to one mm ST segment depression was increased with oxyfedrine as compared to placebo (1.5 +/- 1.5 to 1.9 +/- 1.5 minutes, p less than 0.05). Oxyfedrine did not increase the total duration of exercise (4.1 +/- 1.0 to 4.7 +/- 2.2 minutes, p = NS) or time to ischaemic symptoms (2.7 +/- 1.3 to 2.9 +/- 1.9 minutes, p = NS). The total work done was significantly more on oxyfedrine 312 +/- 189 joules/kg to 370 +/- 209 joules/kg, p less than 0.01) as also the double product achieved (20.6 x 10(3) +/- 6.1 x 10(3) to 22.5 x 10(3) +/- 6.4 x 10(3), p less than 0.01). It is concluded that intravenous oxyfedrine improves exercise capacity in patients with stable effort angina presumably by reducing myocardial ischaemia.

Adult↗
PubMed1975

Potentation of the cardiac response to aminophylline by oxyfedrine.

The influence of oxyfedrine on the cardiostimulatory effects of aminophylline was studied in the isolated perfused guinea-pig heart. It was found that oxyfedrine potentiated the stimulatory effects of aminophylline on isometric contraction, dF/dt, coronary flow and heart rate. This potentation was abolished after pretreatment with propranolol. Histamine, though to a lesser extent, also potentiated the effects of aminophylline. When oxyfedrine and histamine were infused simultaneously in the presence of propranolol, the response of the heart to aminophylline was also potentiated; the magnitude of this potentiation was comparable to that obtained with histamine alone, indicating that propranolol abolished only the action of oxyfedrine but not that of histamine. The mechanical effects of aminophylline were accompanied by a slight (15 per cent) but significant inhibition of phosphodiesterase, which was not further augmented by oxyfedrine. The results suggest that the potentiating effects of oxyfedrine or histamine on the cardiostimulatory actions of aminophylline are elicited by their stimulatory actions on adenylate cyclase activity.

Aminophylline↗
PubMed1975

Positive and negative chronotropic response of the S-A node to oxyfedrine.

Direct perfusion of the sinus node artery under a constant pressure of 100 mmHg was carried out in vagotomized dogs. "Selective" injection of L-3-methoxy-omega-(1-hydroxy-1-phenylisopropylamino) propiophenone hydrochloride (oxyfedrine) into the sinus node artery induced three types of chronotropic response; a pronounced sinus tachycardia, an initial bradycardia followed by sustained tachycarcia, or a definite sinus bradcardia alone. The paradoxical sinus bradycardia induced by oxyfedrine was more pronounced at higher doses of the compound, whereas it was nver produced by the injection of isoproterenol. The oxyfedrine-induced sinus tachycardia, which occurred even in reserpinized preparations, was not suppressed by the treatment with tetrodotoxin, hexamethonium or bretylium, but it was selectively inhibited by propranolol. Atropine, tetrodotoxin or hexamethonium did not prevent the occurrence of sinus bradycardia induced by oxyfedrine, and physostigmine failed to enhance the response. The present study indicates that the oxyfedrine-induced tachycardia is mediated mainly by a direct stimulating action on adrenergic beta-receptors, while the bradycardia appears to be induced by a direct depressant action on the S-A node.

Animals↗
PubMed1982

[Effects of oxyfedrine on sinus nodal function and AV-conduction (author's transl)].

In 20 patients the electrophysiologic effects of oxyfedrine at doses of 0.3 mg/kg/hr and 0.6 mg/kg/hr were studied. At the low dose, oxyfedrine caused a significant shortening of the absolute and rate-corrected sinus node recovery time by 16 and 27 percent, respectively. Sinus cycle length decreased slightly by 9 percent. Estimated sinoatrial conduction time tended to shorten, but not significantly so. AV-nodal conduction was slightly accelerated at sinus rhythm as well as during atrial stimulation; correspondingly paced cycle length at which Wenckebach AH-conduction occurred decreased. HV-interval remained unchanged. Increasing the dose of oxyfedrine had no additional effect on electrophysiologic parameters compared to the first dose used. The results demonstrate a moderate stimulatory action of oxyfedrine on sinus nodal automaticity and a slight acceleration of AV-nodal conduction. Whether the drug might be useful in the clinical setting for medical management of sinus nodal dysfunction or AV-conduction disturbances, remains to be elucidated on long-term studies; more pronounced effects of oxyfedrine than found in this investigation, however, are expected to be limited by its autoinhibitory action at higher dose levels.

Adult↗
PubMed1985

Comparison of oxyfedrine and atenolol in angina pectoris--a double-blind study.

We have compared oxyfedrine 24 mg four times daily with atenolol 100 mg once daily in the relief of angina pectoris in a double-blind cross-over study; assessments were by diary cards and treadmill testing. Both oxyfedrine and atenolol reduced the frequency of angina by similar amounts and both produced similar improvements in treadmill performance. Side effects were infrequent and minor with both drugs. The model of action of oxyfedrine appears to be different from atenolol. Oxyfedrine allows the double product of systolic blood pressure X heart rate at peak exercise to be maintained at levels similar to those with placebo; the double product at peak exercise is significantly less with atenolol.

Adult↗
PubMed1981

Echocardiographic evaluation of acute administration of oxyfedrine in patients with coronary artery disease.

In order to assess the effects of oxyfedrine in ischaemic heart disease, echocardiographic evaluation of left ventricular function was performed 2,5,10,15 and 20 minutes after the intravenous administration of 12 mg oxyfedrine in 15 patients with coronary artery disease without angiographic abnormalities of left ventricular wall motion. The following parameters were measured: heart rate, mean arterial blood pressure, internal dimension in diastole (LVIDd) and in systole (LVIDs) of the left ventricule and the percentage shortening of the LVID (%LVID). There was a significant increase in %LVID (peak 10 minutes after drug administration; p less than 0.001) indicating improved left ventricular function, associated with slight changes in pre-load (LVIDd) and in heart rate, and no variation in mean blood pressure. No abnormalities of contraction were observed after the administration of oxyfedrine. These results suggest that oxyfedrine exerts a direct positive inotropic effect of the myocardium in patients with significant coronary artery stenoses.

Aged↗
PubMed1975

[Stability of oxyfedrine in pharmacological experiments in vitro].

15% of L-3-(beta-hydroxy-alpha-methyl-phenethyl-amino)-3'-methoxy-propiophenone-hydrochloride (oxyfedrine [OF]; ildamen¿) are degradated in Krebs-Henseleit solution under conditions which are necessary for recording a complete concentration-effect curve on guinea-pig papillary muscle (total time max. 100 min). Norephedrine and 3-methoxyacrylophenone are qualitatively analysed as products of degradation by thin-layer chromatography (TLC). Secondary reaction products of the primary degradation are not detectable under these conditions. The quantitative analysis of oxyfedrine, norephedrine and 3-methoxyacrylophenone was carried out by spectrophotometry. Comparatively oxyfedrine and norephedrine were analysed by direct quantitative TLC (measuring of reflectance). The same results were obtained, in principle, by both methods. The importance of this relatively slow degradation for pharmacological in vitro experiments on the mode of action of oxyfedrine is pointed out.

Chromatography, Thin Layer↗
PubMed1985

Double-blind crossover clinical trial of oxyfedrine and propranolol in angina pectoris.

The comparative efficacy and safety of oxyfedrine and propranolol in the management of angina pectoris was evaluated in a double-blind randomized cross-over study. Out of 21 patients registered, 14 completed the study. Three patients dropped out due to poor response and 4 were lost to follow up. Both the drugs i.e. oxyfedrine (8-24 mg three times a day) and propranolol (40-80 mg three times a day) produced a significant reduction in the incidence of anginal attacks and the consumption of nitroglycerine tablets. Propranolol produced a better response than oxyfedrine although the difference was not significant. This may be due to the small sample size. No change in heart rate and rate-pressure product was observed with oxyfedrine, in contrast to that seen with propranolol. The beneficial effect of treatment on exercise tolerance and ST-segment depression was more marked with propranolol. No significant change in laboratory parameters was observed with either drug.

Angina Pectoris↗
PubMed1984

[The importance of increased prostaglandins and prostacyclin for the effect of oxyfedrin in isolated guinea pig heart preparations].

In isolated perfused heart preparations of guinea pigs coronary dilating and positive inotropic doses of oxyfedrine induce a significant increase of the release of prostaglandin-like substances (PLS) and prostacyclin (PGI2). Indometacin as an inhibitor of prostaglandin biosynthesis (140 mumol/l) enhances after a 10 min lasting perfusion contraction force and coronary flow of the hearts but inhibits PGI2-formation. Under these conditions oxyfedrine loses its positive influence on inotropism, coronary flow and PGI2-efflux. Indometacin (140 mumol/l) also completely abolishes the increase of cardiac performance of isolated auricle preparations by oxyfedrine (50 mumol/l). These findings agree with former results and indicate an involvement of the PLS- and PGI2-biosynthesis in the antianginal efficacy of oxyfedrine.

Animals↗
PubMed1978

[The effect of oxyfedrine and intervall training in intermittent claudication (author's transl)].

In 23 patients suffering from intermittent claudication due to chronic occlusions of the femoral artery proved on angiography, a double-blind study was performed to compare the effects of treatment with oxyfedrine and interval-training and of interval-training alone. The claudication distance, physical work capacity and physical work intensity were measured on the treadmill before, during and after 10-weeks training period in each case. After training, the walking ability improved in both groups, however, quantitatively being more pronounced in the oxyfedrine group. In the placebo group, the increase in physical work intensity was mainly caused by the improvement of walking ability in patients with higher levels of performance at the beginning of the training. In the oxyfedrine group, on the other hand, a continuous and regular increase in physical work intensity was found at all levels of performance and during the whole training period. For the differences found, blood supply lowering mechanisms after physical training and improvement of collaterals after combination oxyfedrine and physical training are discussed. The possibility of additive action of the pharmacologic treatment and physical training are pointed out.

Aged↗