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At least 19 recordsLinked to original sources
PubMed1980

Metabolism of vincamine in the rat in vivo and in vitro.

Metabolism of vincamine has been studied in rats in vivo and in vitro using tritium labelled vincamine. Radioactivity was excreted with urine and faeces in an amount of about 62% during 72 h after i.v., i.p. and p.o. administration of the drug. From bile about 40% radioactivity could be recovered during 6 h following i.p. administration. Vincamine is excreted in unchanged form in an amount of 4-6%. In an in vitro system containing rat liver homogenate 6 alpha- and 6 beta-hydroxy-vincamine are formed, as their structures could be deduced from the mass spectrometric data. Rat plasma probably hydrolizes vincamine to vincaminic acid, but the presence of vincaminic acid could not be demonstrated, neither in urine nor in bile. Mass spectrometric investigations of the urinary and biliary metabolites have shown that beyond 6 alpha- and 6 beta-hydroxy-vincamine, their further oxidized form, 6-keto-vincamine also appears. 6 alpha-, 6 beta-hydroxy-vincamine, 6-keto-vincamine and vincamine are eliminated with urine and bile in part as conjugates. Among the metabolites (+)-eburnamonine (vincamone) was also found, which is supposed to be the degradation product of vincaminic acid. The identified compounds are responsible for about 70% of urinary and 30% of biliary radioactivities.

Animals↗
PubMed1977

[Plasma concentrations and renal excretion of vincamine after oral administration in man (author's transl)].

Plasma concentrations and renal excretion of 14,15-dihydro-14beta-hydroxy-(3alpha,16alpha)-eburnamenine-14-carbonic acid methylester (vincamine, Vincapront) were studied in 5 healthy volunteers following the oral intake of 30 or 60 mg vincamine, respectively. After the higher dose (60 mg vincamine), the treatment was continued by the daily intake of 3 X 20 mg vincamine for 5 days. Plasma vincamine levels were determined in the morning prior to the ingestion of the first 20-mg dose and in the evening 2 h after the intake of the third 20-mg dose. Our results prove that vincamine is rapidly liberated and absorbed from the tablet formulation used, the maximum plasma levels being reached 90 min after ingestion and amounting to a mean value of 139 ng/ml after 30 mg and to a mean of 252 ng/ml after 60 mg of vincamine. There was a biphasic elimination of vincamine after both doses indicating a process of distribution influencing also the elimination phase. In the 24-h urine, unchanged vincamine amounted to 5.8% of the applied dose after 30 mg and to 7.3% after 60 mg vincamine. Vincamine did not accumulate during the daily intake of 60 mg for 6 days. Side-effects were not observed in any volunteer during the period of observation.

Administration, Oral↗
PubMed1989

Trachealis responses induced by vincamine and vinpocetine; inhibition by indomethacin and Ca2+ dependence.

Vincamine in low concentrations induced a sustained contraction of the isolated guinea pig trachealis with long latency and slow onset and, in high concentrations, it induced relaxation which was potentiated in the precontracted trachealis. Vinpocetine had actions similar to those of vincamine on trachealis, however its relaxant effect was more pronounced. The vincamine-induced trachealis contraction was not changed by substance P desensitization, was reduced by tetrodotoxin, nifedipine and low Ca2+ high Mg2+ solution and increased in nominally Ca2+-free solution. The vincamine-induced relaxation of precontracted trachealis was increased by guanethidine and was not affected by propranolol, high Mg2+-low Ca2+ solution and tetrodotoxin. Vincamine- and vinpocetine-induced trachealis contraction as well as vinpocetine-induced relaxation at basal tension were abolished by indomethacin. Vincamine in a low concentration shifted to the left the concentration-effect curve for CaCl2 in the K+-depolarized trachealis, and shifted it to the right at a high concentration. Our results indicate that the contractile and relaxant actions of vincamine and vinpocetine on the guinea pig trachealis may be due to the generation of prostaglandins and to changes in the membrane Ca2+ fluxes and/or the intracellular Ca2+ distribution.

Acetylcholine↗
PubMed1979

Comparative study of the clinical effect of vincamine versus papaverine given parenterally in the acute phase of stroke.

The efficacy of the "oxygenator", vincamine was assessed in comparison to a classic vasodilator, papaverine, after parenteral administration during the first days of an acute thrombo-embolic stroke. All 263 patients admitted to this open trial had a thrombo-embolism of the A. carotis or one of its cerebral branches within the previous 24 h. Patients demonstrating minimal neurological deficit or requiring admission to an intensive care unit, or patients with a suspected hemorrhagic syndrome were excluded. Each patient received i.v. infusions (15 mg X 6) of 6 vials of vincamine per 24 h, or 6 vials of papaverine (40 mg X 6) per 24 h, occasionally in combination with acetylsalicylic acid (ASA), dipyridamol and hydrocortisone. An initial 3-h control was followed by regular surveillance for 5 days, paying special regard to consciousness and motricity. The administration of vincamine alone had a significantly more favourable effect than papaverine alone on consciousness (p less than 0.001). Furthermore, vincamine associated with other drugs was significantly superior (p less than 0.01) to papaverine given in association. A similar tendency was noted for motor recuperation after vincamine compared to papaverine (p less than 0.001). Vincamine and papaverine were well tolerated during the 5-days observation period, only one side effect after vincamine and four after papaverine being noted.

Adult↗
PubMed1982

Vincamine: a psychogeriatric agent blocking synaptic potentiation in hippocampus.

The action of vincamine on the physiology of the CA1 region of the in vitro hippocampal slice preparation was investigated. At concentrations of 1, 10 and 100 microM, a five-minute perfusion with vincamine did not affect the synaptically-mediated activation of pyramidal neurons evoked by stimulation of the Schaffer-commissural fiber system. The effect of vincamine on the excitability of the pyramidal neurons was investigated by studying its effect on the antidromically-elicited field potential and the input-output relation of Schaffer-commissural fiber input. No effect on either of the two parameters was seen at a concentration of 100 microM of vincamine. Vincamine did, however, attenuate both the post-tetanic (PTP) and long-term potentiation (LTP) evoked by repetitive stimulation of the Schaffer-commissural fiber system. At a concentration of 100 microM of vincamine, PTP was significantly reduced and LTP was almost completely suppressed.

Action Potentials↗
PubMed2005

Measurement and pharmacokinetics of vincamine in rat blood and brain using microdialysis.

Vincamine is an alkaloid compound derived from the Vinca minor plant. Since little is known concerning its pharmacokinetics and appropriate analytical method, this study focuses on its pharmacokinetics as well the possible roles of the multidrug transporter P-glycoprotein on its distribution and disposition. We develop a rapid and sensitive method using a microdialysis coupled with liquid chromatography for the concurrent determination of unbound vincamine in rat blood and brain. Microdialysis probes were simultaneously inserted into the jugular vein toward heart and brain hippocampus of male Sprague-Dawley rats for sampling in biological fluids following the administration of vincamine (10 and 30 mg/kg) through the femoral vein. Samples were eluted with a mobile phase containing methanol-1% diethylamine (pH 7.15) in water (75:25, v/v) and the flow rate of the mobile phase was 0.7 ml/min. Pharmacokinetic parameters of vincamine were derived using compartmental model. The decline of protein-unbound vincamine in the hippocampus and blood suggested that there was rapid exchange and equilibration between the peripheral compartment and the central nervous system. In the presence of cyclosporine, unbound vincamine levels in both blood and brain were significantly increased.

Animals↗
PubMed2005

Stability-indicating methods for determination of vincamine in presence of its degradation product.

Three different stability indicating assay methods are developed and validated for determination of vincamine in the presence of its degradation product (vincaminic acid). The first method is based on the derivative ratio zero crossing spectrophotometric technique using 0.1 N hydrochloric acid as a solvent. In the second method, measurements are based on spectro-densitometric technique using high performance thin-layer chromatography (HPTLC) plates with a developing system consisting of methanol-chloroform-ethyl acetate (2:1:1, v/v/v). The third method depends on high-performance liquid chromatography (HPLC). Separation of vincamine from vincaminic acid using Lichrocart RP-18 column (250 mm x 4.6 mm i.d.) with a mobile phase consisting of acetonitrile-ammonium carbonate (0.01 M) (7:3, v/v) is achieved. The methods showed high sensitivity with good linearity over the concentration ranges of 12 to 48 microg ml-1, 3 to 17 microg/spot, and 2 to 20 microg ml-1 for derivative spectrophotometry, spectro-densitometry and HPLC methods, respectively. The developed methods were successfully applied to the analysis of pharmaceutical formulations containing vincamine with excellent recoveries.

Chromatography, High Pressure Liquid↗
PubMed2000

In vitro-in vivo correlation and comparative bioavailablity of vincamine in prolonged-release preparations.

Developing an in vitro dissolution test that gives good correlation with in vivo data for a particular drug product is an important objective. Available dissolution data of vincamine prolonged-release preparations show different in vitro release behavior at different pH using the conventional dissolution techniques. This does not allow development of an in vitro-in vivo correlation (IVIVC). In the present work, the flow-through cell (FTC) dissolution system (USP apparatus 4) was utilized to compare the release rate of three marketed prolonged-release oral formulations of vincamine; namely, a brand innovator formulation used as the reference and two formulations from different manufacturers as test products. Both the open and closed systems of FTC were used at variable pH. A comparative bioavailability study was then conducted in 16 healthy volunteers for a test versus the reference product by administering a single dose of 60 mg in a crossover design. Vincamine plasma concentrations were analyzed by a sensitive high-performance liquid chromatography (HPLC) method. This was followed by assessment of IVIVC according to level A as specified by USP 23; the absorbed fraction of vincamine was determined using the Wagner-Nelson method. The results indicated that the pH of the medium affects the release rate pronouncedly. The relative bioavailability based on Cmax and AUC0-12 were found to be 83.15% and 84.15%, respectively. Good correlation was obtained between fraction absorbed in vivo and fraction dissolved in vitro by applying the open system of the FTC. This technique gave the most favorable results with regard to the percentage vincamine released and the IVIVC.

Adult↗
PubMed1980

[Severe ventricular arrhythmia following parenteral administration of vincamine. Predisposing factors in 6 cases].

Six patients developed ventricular arrhythmias with parenteral administration of vincamine. Direct intravenous injection was the mode of administration in 2 cases, intravenous infusion in 3 cases (one at very high dosage) and intramuscular injection in 1 case. The same signs of toxicity were observed in al patients:--5 patients had recorded attacks of "torsades de pointe", which recurred in 1 of them when the drug was restarted.--1 patient had syncope and, although an ECG was not recorded at the time, an ECG shortly afterwards showed a long QT interval and R/T ventricular extrasystoles. Symptoms were generally neurological in nature with syncope, cyanosis, and convulsions. Spontaneous regression was observed in 3 cases but in the others the drug had to be stopped and cardiopulmonary resuscitation instituted. None of our patients died of their arrhythmia. In some patients a predisposing factor was found:--metabolic: hypokalaemia (1 case), moderate reduction of potassium pool (1 case), severe reduction of calcium pool (1 case);--pharmacological: previous treatment with fenoxidil (1 case), thioridazine (1 case);--cardiac: congenital long QT interval (Romano-Ward) (1 case), revealed by vincamine administration. Chronic obstructive airways disease with right ventricular strain and atrial fibrillation (1 case) which might have predisposed the patient to "torsades de pointes". Three patients had no predisposing factors apart from their age. "Torsades de pointes" occurred in a pacemaker patient, but pacemaker function was normal. These six cases may be grouped with the other ten or so cases of vincamine toxicity already reported; they carry and additional warning on the use of intramuscular vincamine. Vincamine toxicity is probably a direct effect on the myocardial cells. This fact merits verification by further electrophysiological studies.

Aged↗
PubMedDate not supplied

[Alerting effect of vincamine in rats (author's transl)].

The alerting effect of vincamine, an indole alkaloid of Vinca minor, has been demonstrated using three electropharmacological tests: 1) the sleep-wakefulness cycle of freely moving rats implanted with cortical electrodes, 2) the sleep induced by 200 mg/kg i.v. sodium 4-hydroxy-butyrate (GHB) in the curarized rat, 3) the duration of spindle activity in the E.E.G. of curarized rats provoked by an acute asphyxia in which the E.E.G. activity was abolished for 20 sec. Vincamine increased the total duration of wakefulness at the expense of sleep, decreased the number of phases of paradoxical sleep (PS), increased the latency of the first phase of PS, but had no effects on the sleep-wakefulness cycle in a further test 24 hours after administration. Vincamine induced neither stereotyped behavior nor hypermotility. Vincamine also decreased the duration of GHB-induced sleep and the duration of post-asphyxic spindles. All effects observed were dose dependent. By means of these electropharmacological tests we have been able to discover two further agents which have more potent alerting effects than vincamine: desoxyvincaminamide and N-cyclopropyl-desoxyvincaminamide.

Animals↗
PubMed1977

[The effect of vincamine on cerebral blood flow as a function of application rate (author's transl)].

The effect of infusions of 14,15-dihydro-14beta-hydroxy-(3alpha, 16alpha)-eburamenine-14-carbonic acid methylester (vincamine; Vincopront) on cerebral blood flow (CBF) was investigated by the xenon clearance method. In 12 patients receiving 30 mg vincamine within 35--40 min no significant changes in hemispheric or regional CBF were observed. 14 patients received 40 mg vincamine within 35--40 min: in this group hemispheric CBF was significantly increased (p less than 0.01) when compared to the spontaneous changes observed in a control group. The increase was particularly prominent in poorly supplied brain regions. This effect was proved statistically by regression analysis. In a patient with astrocytoma the tumor-hyperperfusion was diminished by vincamine while the flow to the surrounding brain improved. The results indicate the dependency of the vincamine effect on the rate of application and thereby on the plasma concentration of the drug.

Adult↗
PubMed1986

Disposition kinetics and oral bioavailability of vincamine-loaded polyalkyl cyanoacrylate nanoparticles.

Hexyl cyanoacrylate nanoparticles loaded with vincamine as a drug model were prepared. Disposition kinetics and oral bioavailability of vincamine in rabbits were compared after administration of an aqueous solution of the drug and an aqueous colloidal suspension of nanoparticles. After intravenous administration, total body clearance of vincamine was equal for both dosage forms, but a longer half-life (X 2) and larger distribution volume (X 2) were observed with the suspension of nanoparticles. After oral administration, the bioavailability of vincamine was considerably greater for the drug loaded onto nanoparticles.

Administration, Oral↗
PubMed1996

Therapeutic efficacy of vincamine in dementia.

This trial was performed to investigate the therapeutic efficacy of vincamine in the treatment of primary degenerative and vascular dementia. 152 male and female patients aged between 50 and 85 years from two psychogeriatric centers and two nursing homes were initially included in the trial and screened for eligibility. 142 patients completed the trial. Clinical diagnosis was established according to DSM-III-R criteria. Allocation of the patients to the primary degenerative dementia of the Alzheimer type (DAT) group or the multi-infarct dementia (MID) group was based on computed tomography scans, electroencephalographic findings and the Hachinski Ischemic Score. In a 12-week double-blind treatment either 30 mg vincamine or placebo was given twice daily. Confirmatory statistics included item 2 of the Clinical Global Impression (CGI), the total score of the Sandoz Clinical Assessment Geriatric (SCAG) scale, the subscale 'need for help' of the nurse's rating of geriatric patients (Beurteilungsskala für geriatrische Patienten; BGP) and the total score of the Short Cognitive Performance Test (Syndrom-Kurztest; SKT). In addition, data on tolerance and on therapy response were evaluated based on descriptive statistics. The therapeutic efficacy of vincamine was clearly demonstrated by confirmatory analysis as the drug was statistically significantly superior to placebo in all four target variables. The clinical relevance of the outcome was further underlined by the results of the responder analysis of the variables SCAG, BGP and SKT. Based on the results of this trial, it can be accepted that the therapeutic effect of vincamine is superior to placebo in patients with mild to moderate dementia of degenerative and vascular etiologies.

Aged↗