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J Neurol Sci. 2005 Mar 15;229-230(1):275-84.
Epub 2005 Jan 8.
Effects of vinpocetine on the redistribution of cerebral
blood flow and glucose metabolism in chronic ischemic stroke patients: a
PET study.
Szilagyi G, Nagy Z, Balkay L, Boros I, Emri M, Lehel S,
Marian T, Molnar T, Szakall S, Tron L, Bereczki D, Csiba L, Fekete I, Kerenyi
L, Galuska L, Varga J, Bonoczk P, Vas A, Gulyas B.
National Stroke Center, Department of Vascular Neurology, Semmelweis University,
H-1085 Budapest, Hungary.
The pharmacological effects of the neuroprotective drug vinpocetine, administered
intravenously in a 14-day long treatment regime, on the cerebral blood flow
and cerebral glucose metabolism in chronic ischemic stroke patients (n=13)
were studied with positron emission tomography in a double-blind design.
The regional and global cerebral metabolic rates of glucose (CMR(glc)) and
cerebral blood flow (CBF) as well as vital physiological parameters, clinical
performance scales, and transcranial Doppler parameters were measured before
and after the treatment period in patient groups treated with daily intravenous
infusion with or without vinpocetine. While the global CMR(glc) values did
not change markedly as a result of the infusion treatment with (n=6) or
without (n=7) vinpocetine, the global CBF increased and regional CMR(glc)
and CBF values showed marked changes in several brain structures in both
cases, with more accentuated changes when the infusion contained vinpocetine.
In the latter case the highest rCBF changes were observed in those structures
in which the highest regional uptake of labelled vinpocetine was measured
in other PET studies (thalamus and caudate nucleus: increases amounting
to 36% and 37%, respectively). The findings indicate that a 2-week long
intravenous vinpocetine treatment can contribute effectively to the redistribution
of rCBF in chronic ischemic stroke patients. The effects are most pronounced
in those brain regions with the highest uptake of the drug. |
J Neurol Sci. 2005 Mar 15;229-230(1):219-23.
Epub 2004 Dec 16.
[(11)C]Vinpocetine: a prospective peripheral benzodiazepine
receptor ligand for primate PET studies.
Gulyas B, Halldin C, Vas A, Banati RB, Shchukin E, Finnema
S, Tarkainen J, Tihanyi K, Szilagyi G, Farde L.
Karolinska Institute, Psychiatry Section, Department of Clinical Neuroscience,
Karolinska Hospital, S-17176 Stockholm, Sweden; Karolinska Institute,
Department of Neuroscience, S-171 77 Stockholm, Sweden.
Vinpocetine, a synthetic derivative of the Vinca minor alkaloid vincamine,
is a widely used drug in neurological practice. We tested the hypothesis
that vinpocetine binds to peripheral benzodiazepine binding sites (PBBS)
and is therefore a potential ligand of PBBS. Positron emission tomography
(PET) measurements in two cynomolgous monkeys showed that pretreatment
with vinpocetine markedly reduced the brain uptake of [(11)C]PK11195,
a known PBBS radioligand. On the other hand, whereas pretreatment with
PK11195 increased the brain uptake of [(11)C]vinpocetine due to the blockade
of PBBS in the periphery, it significantly reduced the binding potential
(BP) values of [(11)C]vinpocetine in the whole brain and in individual
brain structures to PK11195. These findings indicate that, whereas the
two ligands have different affinities to PBBS, vinpocetine is a potent
ligand of PBBS, which in turn suggests that the pharmacological activity
of vinpocetine may involve the regulation of glial functions.
|
Ann Neurol 2002 May;51(5):604-12
Impact of sustained deprenyl (selegiline) in levodopa-treated
Parkinson's disease: a randomized placebo-controlled extension of the deprenyl
and tocopherol antioxidative therapy of parkinsonism trial
Shoulson
I, Oakes D, Fahn S, Lang A, Langston JW, LeWitt P, Olanow CW, Penney JB,
Tanner C, Kieburtz K, Rudolph A; Parkinson Study Group
In a double-blind clinical trial, vinpocetine, a synthetic ethyl ester of
apovincamine, was shown to effect significant improvement in elderly patients
with chronic cerebral dysfunction. Forty-two patients received 10 mg vinpocetine
three times a day (tid) for 30 days, then 5 mg tid for 60 days. Matching
placebo tablets were given to another 42 patients for the 90 day trial period.
Patients on vinpocetine scored consistently better in all evaluations of
the effectiveness of treatment including measurements on the Clinical Global
Impression (CGI) scale, the Sandoz Clinical Assessment-Geriatric (SCAG)
scale, and the Mini-Mental Status Questionnaire (MMSQ). There were no serious
side effects related to the treatment drug. |
Clin Neuropharmacol 2002 Jan-Feb;25(1):37-42
In vitro antioxidant properties of pentoxifylline, piracetam,
and vinpocetine
Horvath B, Marton Z, Halmosi
R, Alexy T, Szapary L, Vekasi J, Biro Z, Habon T, Kesmarky G, Toth K
First Department of Medicine Division of Cardiology, Department of Neurology,
and the Department of Ophthalmology, University of Pecs' School of Medicine,
Pecs, Hungary
Oxygen-free radicals play an important role in several physiologic and pathophysiologic
processes. In pathologic circumstances, they can modify and damage biologic
systems. Because oxygen-free radicals are involved in a wide range of diseases
(cerebrovascular, cardiovascular, etc.), scavenging these radicals should
be considered as an important therapeutic approach. In our in vitro study,
we investigated the antioxidant capacity of three drugs: pentoxiphylline
(Sigma Aldrich, St. Louis, MO, USA) piracetam (Sigma Aldrich), and vinpocetine
(Richter Gedeon RT, Budapest, Hungary). Phenazine methosulphate was applied
to generate free radicals, increasing red blood cell rigidity. Filtration
technique and potassium leaking were used to detect the cellular damage
and the scavenging effect of the examined drugs. According to our results,
at human therapeutic serum concentration, only vinpocetine (Richter Gedeon
RT) had significant (p < 0.01) scavenging activity with a protective
effect that increased further at higher concentrations. Pentoxiphylline
(Sigma Aldrich) and piracetam (Sigma Aldrich) did not have significant antioxidant
capacity at therapeutic concentrations, but increasing their concentrations
(pentoxiphylline at 100-times, and piracetam at 10-times higher concentrations)
led to a significant (p < 0.01) scavenger effect. Our findings suggest
that this pronounced antioxidant effect of vinpocetine and even the milder
scavenging capacity of pentoxiphylline and piracetam may be of value in
the treatment of patients with cerebrovascular disorders, but merits further
investigations. |
Neurochem Res 2001 Sep;26(8-9):1095-100
The nootropic drug vinpocetine inhibits veratridine-induced
[Ca2+]i increase in rat hippocampal CA1 pyramidal cells
Zelles
T, Franklin L, Koncz I, Lendvai B, Zsilla G
Institute of Experimental Medicine, Hungarian Academy of Sciences, Budapest
The alkaloid derivative vinpocetine (14-ethoxycarbonyl-(3alpha,16alpha-ethyl)-14,15-eburnamine;
Cavinton) has a well known beneficial effect on brain function in hypoxic
and ischemic conditions. While it increases CNS blood flow and improves
cellular metabolism, relatively little is known about vinpocetine's underlying
molecular mechanisms on the single cell level. Since apoptotic and necrotic
cell damage is always preceded by an increase in [Ca2+]i, this study investigated
the effect of vinpocetine on [Ca2+]i increases in acute brain slices. Sodium
influx is an early event in the biochemical cascade that takes place during
ischemia. The alkaloid veratridine can activate this Na+ influx, causing
depolarization and increasing [Ca2+]i in the cells. Therefore, it can be
used to simulate an ischemic attack in brain cells. Using a cooled CCD camera-based
ratio imaging system and cell loading with fura 2/AM, the effect of vinpocetine
on [Ca2+]i changes in single pyramidal neurons in the vulnerable CA1 region
of rat hippocampal slices was investigated. Preperfusion and continuous
administration of vinpocetine (10 microM) significantly inhibited the elevation
in [Ca2+]i induced by veratridine (10 microM). When the drug was administered
after veratridine, it could accelerate the recovery of cellular calcium
levels. Piracetam, another nootropic used in clinical practice, could attenuate
the elevation of [Ca2+]i only at a high, 1 mM, concentration. We have concluded
that vinpocetine, at a pharmacologically relevant concentration, can decrease
pathologically high [Ca2+]i levels in individual rat hippocampal CA1 pyramidal
neurons; this effect might contribute to the neuroprotective property of
the drug. |
Eur J Neurol 2001 Jan;8(1):81-5
Vinpocetine treatment in acute ischaemic stroke: a pilot
single-blind randomized clinical trial
Feigin
VL, Doronin BM, Popova TF, Gribatcheva EV, Tchervov DV
Department of Epidemiology and Preventive Medicine, Institute of Internal
Medicine, Siberian Branch of the Russian Academy of Medical Science, Novosibirsk,
Russia
The aim of the study was to assess the safety and feasibility of a clinical
trial on the effect of vinpocetine, a synthetic ethyl ester of apovincamine,
in acute ischaemic stroke. Thirty consecutive patients with computed tomography
verified diagnosis of acute ischaemic stroke, who could receive drug treatment
within 72 h of stroke onset, were enrolled. The patients were randomly allocated
to receive either low-molecular weight dextran alone or in combination with
vinpocetine. Poor outcome was defined as being dead or having a Barthel
index of < 70 or a Rankin score of 3--5. Intention-to-treat analysis
was applied. One-tenth of all hospitalized patients with acute ischaemic
stroke were eligible for the trial. Thirty eligible patients were treated
with either low-molecular weight dextran alone (mean age 57.9 +/- 11.6 years,
n = 15) or in combination with vinpocetine (mean age 60.8 +/- 6.6 years,
n = 15). The two treatment groups were comparable with respect to major
prognostic variables. A relative risk (RR) reduction of poor outcome at
3 months follow-up was 30% (RR = 0.7; 95% confidence interval [CI] 0.1--3.4),
as defined by the modified Barthel Index, and 60% as defined by the modified
Ranking score (RR = 0.4, 95% CI: 0.1--1.7). The National Institute of Health
(NIH--NINDS) Stroke Scale score was marginally significantly better in the
vinpocetine treated group at 3 months of follow-up (P = 0.05, ANOVA). No
significant adverse effects were seen. This pilot study shows that a full-scale
randomized double-blind, placebo-controlled trial of vinpocetine treatment
in acute ischaemic stroke is feasible and warranted. |
Free Radic Res 2000 Jan;32(1):57-66
Synaptosomal response to oxidative stress: effect of
vinpocetine
Santos MS, Duarte AI, Moreira PI,
Oliveira CR
Department of Zoology and Faculty of Medicine, Center for Neurosciences
of Coimbra, University of Coimbra, Portugal
It has been suggested that reactive oxygen species (ROS) play a role in
the neuronal damage occurring in ischemic injury and neurodegenerative disorders
and that their neutralization by antioxidant drugs may delay or minimize
neurodegeneration. In the present study we examine whether vinpocetine can
act as an antioxidant and prevent the formation of ROS and lipid peroxidation
in rat brain synaptosomes. After ascorbate/Fe2+ treatment a significant
increase in oxygen consumption (about 5-fold) and thiobarbituric acid reactive
substances (TBARS) formation (about 7-fold) occurred as compared to control
conditions. Vinpocetine inhibited the ascorbate/Fe2+ stimulated consumption
of oxygen and TBARS accumulation, an indicator of lipid peroxidation, in
a concentration-dependent manner. The ROS formation was also prevented by
vinpocetine. Oxidative stress increased significantly the fluorescence of
the probes 2',7'-dichlorodihydrofluorescein (DCFH2-DA) (about 6-fold) and
dihydrorhodamine (DHR) 123 (about 10-fold), which is indicative of intrasynaptosomal
ROS generation. Vinpocetine at 100 microM concentration decreased the fluorescence
of DCFH2-DA and DHR 123 by about 50% and 83%, respectively. We conclude
that the antioxidant effect of vinpocetine might contribute to the protective
role exerted by the drug in reducing neuronal damage in pathological situations. |
Eur J Clin Pharmacol 1992;42(3):257-9
Effects of aspirin, dipyridamole, nifedipine and cavinton
which act on platelet aggregation induced by different aggregating agents
alone and in combination
Akopov SE, Gabrielian
ES
Department of Pharmacology, Yerevan Medical Institute, Armenia
The effects of vinpocetine, a recently described cerebral blood flow enhancer
having antihypoxic, anti-ischemic, and cognitive-function-improving actions,
on rat brain monoaminergic neurotransmission have been studied under normoxic
and hypoxic conditions. Vinpocetine slightly affected the steady-state levels
of monoamines and their metabolites in whole brain, but a tendency was seen
to increase dopamine (DA) and its metabolites in lower brain parts and to
reduce noradrenaline (NA) in "terminal" regions. MHPG-SO4 leveis
were enhanced in whole brain and in almost all regions examined. There was
a tendency to increase S-hydroxyindole-acetic acid (S-HIAA) in some areas.
It accelerated the whole brain NA turnover dose-dependently, but lett that
of DA unchanged. Enhancement of NA turnover was most noted in the lower
brain areas. On the other hand, no change was found in DA accumulation,
an index of heart NA turnover after inhibition of dopamine-beta-hydroxylase.
The rate of probenecide- induced accumulation of cerebral MHPG-SO4 and,
to a lesser extent, that of 5-HIAA was also increased. No change was seen
in the pargyline-induced serotonin (5-HT) accumulation. Although vinpocetine
had slight or no effects on regional levels of monoamines and their metabolites,
and did not alter their in vivo biosynthesis rate under normoxic conditions,
it was able partially or totally to prevent reductions in the biosynthesis
rate of rnonoamines and antagonized the decrease of NA, 5-HT, and 5-HIAA
(but not that of DA) induced by normobaric hypoxia. This effect was mainly
confined to lower brain areas. From the results, we conclude that vinpocetine
primarily aflects cell body regions (e.g., brainstem) of the rat brain.
|
| Arzneimittelforschung
1992 Apr;42(4):425-7
Effect of vinpocetine on red blood cell deformability
in stroke patients
Hayakawa M
Department of Geriatrics, Nagoya University School of Medicine, Japan
Reduction in red blood cell deformability is a contributory factor in
stroke disease, and it has been postulated that red blood cell rigidification
may be improved by drug treatment. In this paper the effect of vinpocetine
(CAS 42971-09-5) on the deformability of red blood cells from patients
with chronic ischemic cerebrovascular disease has been examined. During
the administration of vinpocetine for 3 months a significant improvement
in red blood cell deformability was observed without adverse effect. |
Arzneimittelforschung 1990 Jun;40(6):640-3
Effect of vinpocetine on oxygen release of hemoglobin
and erythrocyte organic polyphosphate concentrations in patients with vascular
dementia of the Binswanger type
Tohgi H, Sasaki
K, Chiba K, Nozaki Y
Department of Neurology, Iwate Medical University, Japan
Oxygen affinity of hemoglobin, erythrocyte 2,3-diphosphoglycerate (DPG)
and adenosine triphosphate (ATP) concentrations were compared before and
after oral administration of vinpocetine (TCV-3B) (15 mg/d), a primarily
vasodilating agent, for three weeks in eight patients with vascular dementia
of the Biswanger type which is characterized by diffuse myelin pallor and
multiple lacunes in the cerebral white matter. After vinpocetine administration,
oxygen affinity of hemoglobin (P50) was significantly increased (26.5 +/-
0.55 to 27.6 +/- 0.62 mmHg; mean and standard deviation, p less than 0.05),
red blood cell (RBC) ATP concentrations were significantly increased (846
+/- 168 to 1,158 +/- 130 mumol/l RBC, p less than 0.05), while DPG concentrations
were unaltered (4.46 +/- 0.48 to 4.59 +/- 0.57 mmol/l RBC). There was a
significant positive correlation between the increase of P50 and the increase
of erythrocyte ATP concentrations (r = 0.67, p less than 0.05). The effect
of vinpocetine of enhancing oxygen release of hemoglobin may offer an additional
benefit to its primary vasodilating action in the treatment of vascular
dementia of the Binswanger type due to chronic ischemia. |
| Drug Develop Res 1988;
14: 191-3
Possible Memory-Enhancing Properties of Vinpocetine
Donna M. Coleston and Ian Hindrnarch
Human Psychopharmacology Research Unit, Department of Psychology, University
of Leeds, Leeds, England
Critical flicker fusion threshold, choice reaction time, total reaction
time, and Sternberg-type mernory tasks of digits/words were measured in
twelve volunteers after having received vinpocetine or placebo for two
days. A significant improvement was recorded in the short-terrn memory
test following 40 mg of the drug when cornpared to placebo. |
Drug Develop Res 1988; 14: 263-79
On the Possible Role of Central Monoaminergic Systems
in the Central Nervous System Actions of Vinpocetine
Bela
Kiss and Laszlo Szporny
Department of Biochemistry, Pharrnacological Research Centre, Chemical Works
of Gedeon Richter Lld., Budapest, Hungary
The effects of vinpocetine, a recently described cerebral blood flow enhancer
having antihypoxic, anti-ischemic, and cognitive-function-improving actions,
on rat brain monoaminergic neurotransmission have been studied under normoxic
and hypoxic conditions. Vinpocetine slightly affected the steady-state levels
of monoamines and their metabolites in whole brain, but a tendency was seen
to increase dopamine (DA) and its metabolites in lower brain parts and to
reduce noradrenaline (NA) in "terminal" regions. MHPG-SO4 leveis
were enhanced in whole brain and in almost all regions examined. There was
a tendency to increase S-hydroxyindole-acetic acid (S-HIAA) in some areas.
It accelerated the whole brain NA turnover dose-dependently, but lett that
of DA unchanged. Enhancement of NA turnover was most noted in the lower
brain areas. On the other hand, no change was found in DA accumulation,
an index of heart NA turnover after inhibition of dopamine-beta-hydroxylase.
The rate of probenecide- induced accumulation of cerebral MHPG-SO4 and,
to a lesser extent, that of 5-HIAA was also increased. No change was seen
in the pargyline-induced serotonin (5-HT) accumulation. Although vinpocetine
had slight or no effects on regional levels of monoamines and their metabolites,
and did not alter their in vivo biosynthesis rate under normoxic conditions,
it was able partially or totally to prevent reductions in the biosynthesis
rate of rnonoamines and antagonized the decrease of NA, 5-HT, and 5-HIAA
(but not that of DA) induced by normobaric hypoxia. This effect was mainly
confined to lower brain areas. From the results, we conclude that vinpocetine
primarily aflects cell body regions (e.g., brainstem) of the rat brain.
|
J Am Geriatr Soc 1987 May;35(5):425-30
A double-blind placebo controlled evaluation of the
safety and efficacy of vinpocetine in the treatment of patients with chronic
vascular senile cerebral dysfunction
Balestreri
R, Fontana L, Astengo F
University of Rochester Medical Center, Rochester, NY 14620, USA
Deprenyl (selegiline) delays the need for levodopa therapy in patients with
early Parkinson's disease, but the long-term benefits of this treatment
remain unclear. During 1987 to 1988, 800 patients with early Parkinson's
disease were randomized in the Deprenyl and Tocopherol Antioxidative Therapy
of Parkinsonism trial to receive deprenyl, tocopherol, combined treatments,
or a placebo and were then placed on active deprenyl (10mg/day). A second,
independent randomization was carried out in early 1993 for 368 subjects
who by that time had required levodopa and who had consented to continuing
the deprenyl treatment (D subjects) or changing to a matching placebo (P
subjects) under double-blind conditions. The first development of wearing
off, dyskinesias, or on-off motor fluctuations was the prespecified primary
outcome measure. During the average 2-year follow-up, there were no differences
between the treatment groups with respect to the primary outcome measure
(hazard ratio, 0.87; 95% confidence interval, 0.63, 1.19; p = 0.38), withdrawal
from the study, death, or adverse events. Although 34% of D subjects developed
dyskinesias and only 19% of P subjects did (p = 0.006), only 16% of D subjects
developed freezing of gait but 29% of P subjects did (p = 0.0003). Decline
in motor performance was less in D subjects than P subjects. Levodopa-treated
Parkinson's disease patients who had been treated with deprenyl for up to
7 years, compared with patients who were changed to a placebo after about
5 years, experienced slower motor decline and were more likely to develop
dyskinesias but less likely to develop freezing of gait. |
| Eur J Clin Pharmacol
1985;28(5):567-71
Psychopharmacological effects of vinpocetine in normal
healthy volunteers
Subhan Z, Hindmarch I
Twelve healthy female volunteers received pre-treatments with vinpocetine
10, 20, 40 mg and placebo (t.d.s.) for two days according to a randomised,
double-blind crossover design. On the third day of treatment and 1 h following
morning dosage, subjects completed a battery of psychological tests including
Critical Flicker Fusion (CFF), Choice Reaction Time (CRT), Subjective
Ratings of Drug Effects (LARS) and a Sternberg Memory Scanning Test. No
statistically significant changes from placebo were observed on CFF, CRT
or subjective ratings of drug effects. However, memory as assessed using
the Sternberg technique was found to be significantly improved following
treatment with vinpocetine 40 mg when compared to placebo and results
suggested a localised effect of the drug on the serial comparison stage
of the reaction process. |
| Advances in therapy
1985; 2:53-6
Effect of Vinpocetine on Cerebral Blood Flow in Patients
with Cerebrovascular Disorders
Norihiko Tamaki, M.D. Tadaki Kusunoki, M.D. Satoshi
Matsumoto, M.D.
Department of Neurosurgery. Kobe University School of Medicine. Kobe,
Japan
The 133xenon inhalation method was used in an open-label clinical trial
to examine changes in cerebral blood flow (CBF) after vinpocetine treatment
in 13 patients with cerebrovascular disorders. In all patients, measurement
of regional cerebral blood flow (RCBF) was made prior to and after treatment
with vinpocetine 5 mg t.i.d. for five to seven weeks. In ten of the patients,
treatment was continued for a total of 8 to 16 weeks with an additional
RCBF measurement at the end of their treatment. The resulte showed a significant
increase in the Initial Slope Index (ISI) values of mean total CBF, and
RCBF for the involved hemisphere after six weeks of treatment with vinpocetine.
The CBF for the involved lobe was significantly increased for ISI and
flow rate of gray matter at six weeks and at the end of treatment. No
adverse reactions were reported. |
Arzneimittelforschung 1976;26(10a):1945-7
Effect of ethyl apovincaminate on the cerebral circulation.
Studies in patients with obliterative cerebral arterial disease
Solti F, Iskum M, Czako E
The effect of ethyl apovincaminate (RGH-4405, Cavinton) on the cerebral
and systemic circulations has been studied in detail in ten cases of cerebrovascular
disease. 10 mg doses of Cavinton were given as infusion within 4-6 min;
circulatory tests were carried out prior to administration of the drug and
3-6 min after. The principal results showed the following: On Cavinton cerebral
vascular resistance was strongly reduced, while cerebral fraction of cardiac
output significantly increased. On acute effect of the drug arterial mean
pressure slightly decreased but cerebral blood flow nevertheless increased
in general. Total vascular resistance also decreased but this decrease was
less marked than that registered in cerebral vascular resistance. |
| |
|
Drug information |
|
| Brand name: Vinpocetine
®
Other popular brand names: Intelectol ®
1. DESCRIPTION: Vinpocetine is a semi-synthetic derivative
of vincamine. Vincamine is an alkaloid derived from the plant Vinca minor
L., a member of the periwinkle family. Vinpocetine, as well as vincamine,
are used in Europe, Japan and Mexico as pharmaceutical agents for the
treatment of cerebrovascular and cognitive disorders. In the United States,
vinpocetine is marketed as a dietary supplement. It is sometimes called
a nootropic, meaning cognition enhancer, from the Greek noos for mind.
Vinpocetine is also known as ethyl apovincaminate; ethyl apovincaminoate;
eburnamenine-14-carboxylic acid ethyl ester; 3 alpha, 16 alpha-apovincaminic
acid ethyl ester; ethyl apovincamin-22-oate; and cavinton, which is sometimes
used generically for a branded product with that name. Another vinca alkaloid
called vinconate is also being researched as a possible cognition enhancer.
The structural formula of vinpocetine is:
2. PHARMACOLOGY: Vinpocetine has several possible actions,
including increasing cerebral blood flow and metabolism, anticonvulsant,
cognition enhancement, neuroprotection and antioxidant. Vincamine, the
parent compound of vinpocetine, is believed to be a cerebral vasodilator.
3. MECHANISM OF ACTION: Several mechanisms have been
proposed for the possible actions of vinpocetine. Vinpocetine has been
reported to have calcium-channel blocking activity, as well as voltage-gated
sodium channel blocking activity. It has also been reported to inhibit
the acetylcholine release evoked by excitatory amino acids and to protect
neurons against excitotoxicity. In addition, vinpocetine has been shown
to inhibit a cyclic GMP phosphodiesterase, and it is speculated that this
inhibition enhances cyclic GMP levels in the vascular smooth muscle, leading
to reduced resistance of cerebral vessels and increase of cerebral flow.
In some studies, vinpocetine has demonstrated antioxidant activity equivalent
to that of vitamin E.
4. PHARMACOKINETICS: Vinpocetine is absorbed from the
small intestine, from whence it is transported to the liver via the portal
circulation. From the liver via the systemic circulation, it is distributed
to various tissues in the body, including the brain. Absorption of vinpocetine
is significantly higher when given with food and can be up to about 60%
of an ingested dose. On an empty stomach, absorption of an ingested dose
can be as low as 7%. Peak plasma levels are obtained one to one and a
half hours after ingestion. Extensive metabolism to the inactive apovincaminic
acid occurs in the liver. Only small amounts of unmetabolized vinpocetine
are excreted in the urine, the major route of excretion of apovincaminic
acid. Most of a dose is excreted within 24 hours as this metabolite. The
elimination half-life of vinpocetine following ingestion is one to two
hours.
5. INDICATIONS AND USAGE: The primary claim made for
vinpocetine is that it decreases fatality and dependency in ischemic stroke.
Research results are mixed. Vinpocetine has not been helpful in Alzheimer's
disease, but there is some suggestion that it might help some with other
dementias and cerebral dysfunction. Very preliminary research additionally
suggests that vinpocetine may help protect the eye and ear from injuries
caused by trauma (and, in the case of the eye, from infection) and that
it might be gastroprotective, ameliorate symptoms of motion sickness and
help prevent atherosclerosis.
6. RESEARCH SUMMARY: Several small studies, in both
animals and humans, have reported significant vinpocetine-associated protective
effects in ischemic stroke. A review of these studies, however, found
only one positive study of a truly randomized, unconfounded clinical trials
that compared the effect of vinpocetine to either placebo or another reference
treatment for acute stroke where treatment started no later than 14 days
after stroke onset. There is currently not enough evidence to determine
whether vinpocetine does or does not reduce fatalities and dependence
in ischemic stroke. Further research is needed.
There is some evidence vinpocetine may be useful in some other cerebral
maladies. In one multi-center, double-blind, placebo-controlled study
lasting 16 weeks, 203 patients described as having mild to moderate psychosyndromes,
including primary dementia, were treated with varying doses of vinpocetine
or placebo. Significant improvement was achieved in the vinpocetine-treated
group as measured by "global improvement" and cognitive performance
scales. Three 10-milligram doses daily were as effective or more effective
than three 20-milligram doses daily. Similarly good results were found
in another double-blind clinical trial testing vinpocetine versus placebo
in elderly patients with cerebrovascular and central nervous system degenerative
disorders. Studies of Alzheimer's disease, however, have shown no vinpocetine
benefit.
Some preliminary research suggests that vinpocetine may have some protective
effects in both sight and hearing. One study of patients with mild burn
trauma in the eyes showed that vinpocetine enhanced healing, most likely
as a result of increased blood flow to the damaged tissue. Vinpocetine
has also been associated with improvements seen in retinas damaged by
hepatitis B virus. Damage from acoustic trauma has similarly been reduced
by vinpocetine treatment.
Vinpocetine gastroprotective effects have been reported in animal models
challenged with noxious agents. There are anecdotal reports that vinpocetine
is protective against some of the gastric and neurological toxicity of
excessive alcohol consumption.
There are some reports that vinpocetine may be an effective motion sickness
preventative and some early findings in animals that it may exert some
anti-atherosclerotic effects through a reported ability to decalcify cholesterol-induced
atherosclerotic lesions.
7. CONTRAINDICATIONS: None known.
8. PRECAUTIONS: Pregnant women and nursing mothers should
avoid vinpocetine supplements. Those with a history of allergic reactions
or hypersensitivity reactions during treatment with other vinca alkaloids,
such as vinblastine and vincristine, should avoid vinpocetine. Those on
warfarin are advised to have their INRs (international normalized ratios)
regularly monitored when using vinpocetine supplements (see Interactions).
Those with hypotension or orthostatic hypotension should be cautioned
that prolonged use of vinpocetine may lead to slight reductions in systolic
and diastolic blood pressure.
9. ADVERSE REACTIONS: Reported adverse reactions include
nausea, dizziness, insomnia, drowsiness, dry mouth, transient hypotension,
transient tachycardia, pressure-type headache and facial flushing. Slight
reductions in both systolic and diastolic blood pressure with prolonged
use of vinpocetine have been reported, as well as slight reductions in
blood glucose.
10. INTERACTIONS: Warfarin—Slight changes in prothrombin
time have been noted in those adding vinpocetine to warfarin dosing. The
changes appear minimal. However, regular monitoring of INR is advised
in those using warfarin and vinpocetine concomitantly. There are no other
known drug or nutritional supplement, herb or food interactions.
11. OVERDOSAGE: There are no reports of vinpocetine
overdosage.
12. DOSAGE AND ADMINISTRATION: Vinpocetine is available
as an individual supplement and in combination products. Typical doses
for supplement use are 5 to 10 milligrams daily with food. Some take up
to 20 milligrams daily. Higher doses are not advised.
Caution!Before starting
to take this medicine, it is vital that you should consult your doctor!
Do not use it on your own initiative, without medical advice.
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Order now ! |
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VINPOCETINE 5 mg
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Dosage |
Packing |
Price |
Pay now |
5 mg |
50 tab |
USD 13.00 |
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5 mg |
100 tab |
USD 22.00 |
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5 mg |
150 tab |
USD 29.00 |
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Dosage |
Packing |
Price |
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10 mg |
30 tab |
USD 14.00 |
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10 mg |
90 tab |
USD 37.00 |
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