Scientific Name(s):Ethyl-apovincaminate 1 , 2

Common Name(s): Vinpocetine , Cavinton , apovincaminic acid kavinton 1 , 3 , 4


The scientific literature contains numerous studies and investigations on the pharmacological and biochemical actions of vinpocetine, including antioxidant effects, menopause, antiulcer activity, and phosphodiesterase-1 inhibition. Vinpocetine is best known for its neuroprotective effects. However, there are limited clinical studies to support the use of vinpocetine for many of these potential uses.


Follow suggested manufacturers' product guidelines. Most clinical studies used vinpocetine 10 mg 3 times daily, orally or parenterally.


The drug should not be used in patients with severe, general, cerebral hypertensive crises, or in elderly or senile patients with acute cardio-cerebral or cerebro-cardiac syndrome, postinfarction cardiosclerosis, or marked disorders of heart rhythm. 5


Avoid use during pregnancy and lactation because of lack of clinical studies.


Caution is warranted in patients on blood-thinning medications because vinpocetine decreases platelet aggregation. In 1 study, bioavailability increased 60% to 100% when vinpocetine was taken with food.

Adverse Reactions

One review article documents patients reporting flushing, rashes, and minor GI problems.


None well documented in the scientific literature.


Vinpocetine is synthesized from the alkaloid vincamine, which is extracted from the leaves of the periwinkle plant Vinca minor . 1 , 6


Vinpocetine was synthesized in the late 1960s and has been sold under the commercial name Cavinton since 1978. Cavinton has been used for nearly 27 years and is available in 47 countries, including Japan, Hungary, Germany, Poland, and Russia. 1 , 6 Vinpocetine is primarily used in treating cerebral disorders of vascular origin. 1 , 5 , 7


Review of the scientific literature reveals few chemical studies of vinpocetine, except for those analyzing its synthesis from the alkaloid vincamine. High-performance liquid chromatography determined apovincaminic acid as the primary metabolite of vinpocetine. 1 , 3

Uses and Pharmacology

The scientific literature contains numerous studies and investigations on the pharmacological and biochemical actions of vinpocetine. The various mechanism of actions include: 1) effects on brain circulation and oxygen utilization without changes in systemic circulation; 2) increased tolerance of the brain to vascular hypoxia and ischemia; 3) anticonvulsant activity; 4) phosphodiesterase-1 inhibition; and 5) lowering of blood viscosity and inhibition of aggregation of thrombocytes. 7

Antioxidant effects
In vitro and animal data

Vinpocetine has a scavenger effect similar to that of vitamin E. Its antioxidant activity also was tested in vitro against pentoxifylline and piracetam; vinpocetine had significant ( P  < 0.01) scavenging activity compared with these drugs. It demonstrated glioprotective activity during and after in vitro stimulated hypoxia in an astrocyte cell culture model. In animal models, vinpocetine inhibited the formation of reactive oxygen species and lipid peroxidation in rat brain synaptosomes. 8 , 9 , 10 , 11 , 12

Clinical data

The therapeutic effect of Cavinton (vinpocetine) on menopausal complaints was assessed in 3 groups of women (control or group 1 [n = 30], group 2 with normolipidemia [n = 32], and group 3 with hyperlipidemia [n = 29]) in early menopause. Primary outcome measurements included: relief of climacteric symptoms assessed by the Kupperman menopausal index and the Hamilton Anxiety Scale (HAMA); and any changes in lipid metabolism (total cholesterol, HDL- and LDL-cholesterol, triglycerides, and 2 indexes of lipid atherogenic risk-total/HDL-cholesterol ratio and atherogenic index [AI] = total-HDL/LDL-cholesterol). Groups 2 and 3 received an oral dose of Cavinton 5 mg 3 times daily for 3 months. Kupperman index and HAMA scores decreased significantly on day 45 and in the third month in groups 2 and 3. A statistically significant decrease in total cholesterol and LDL-cholesterol levels was observed in group 3. 13

A comparative investigation involving 40 climacteric postmenopausal women studied the effects of hormone substitution therapy and combined hormone substitution and Cavinton adjuvant therapy. Relief or improvement of climacteric symptoms was measured by the Kupperman index. The results were statistically analyzed, and Cavinton appeared to improve symptoms experienced with estrogen substitution. 14

Antiulcer activity
Animal and in vitro data

The efficacy of vinpocetine against several agents that cause gastric mucosal damage was studied in rats. Oral and intraperitoneal administration of vinpocetine inhibited development of dose-dependent gastric lesions caused by 96% ethanol. Vinpocetine provided the most protection when given intraperitoneally 30 minutes before ethanol. It demonstrated activity against gastric injury induced by phenylbutazone, chronic gastric ulcer induced by acetic acid, and histamine-stimulated gastric acid secretion in pylorus-ligated rats. The antiulcer activity and protective effect of vinpocetine was compared with that of prostaglandin E2, sucralfate, and tripotassium dicitrate bismuthate. 15

Phosphodiesterase-1 inhibition

Vinpocetine inhibits calcium calmodulin-dependent phosphodiesterase (PDE) type 1. This inhibition may lead to increases in cyclic adenosine 3′,5′-monophosphate and may be responsible for benefits in cerebral circulation and decreased platelet aggregation. 1

Animal and in vitro data

Vinpocetine potentiated the effect of sodium nitroprusside and nitroglycerin on the smooth muscle cells in a rat aorta model. Vinpocetine produced a dose-dependent inhibition on Ca2+ conductivity and decreased the smooth muscle contractility of the membrane at a concentration of 2 to 20 microM. PDE activity was inhibited at a concentration of 1 microM. 16

In an in situ-perfused, rat lung preparation, vinpocetine attenuated acute hypoxic vasoconstriction. 17

Clinical data

Vinpocetine was investigated in nonresponders to standard pharmacological therapy for urge incontinence and low compliance bladder. In 11 of 19 patients, clinical symptoms were improved. Vinpocetine may also have a potential role in the treatment of urgency and interstitial cystitis. 18 , 19

Neuroprotective effects
Animal data

Vinpocetine 2 mg/kg prevented hearing loss induced by the aminoglycoside antibiotic amikacin 450 mg/kg in guinea pigs. 20

Clinical data

Details of the study are limited, but Cavinton prevented neurosensory hypoacusis in 118 tuberculosis patients (17 to 63 years of age) who had normal hearing or hearing problems. 21

Antiepileptic activity

Mechanism of action may involve blockade of presynaptic sodium and calcium channels. Brain gamma-aminobutyric acid and serotonergic mechanisms may be involved. 22 , 23

Animal data – Vinpocetine protected mice against convulsions induced by corazol, strychnine, and thiosemicarbazide. It also antagonized the convulsive reactions produced by systemic administration of penicillin or combined administration of penicillin with a tryptophan metabolite (quinolinic acid) in cats. 23 In guinea pigs, vinpocetine 2 to 10 mg/kg inhibited tonic-clonic convulsions and auditory alterations induced by pentylenetetrazole 100 mg/kg. Vinpocetine 2 mg/kg completely prevented electroencephalogram (EEG) changes induced by pentylenetetrazol for the ictal and postictal periods when administered prior to pentylenetetrazol. 24

Vinpocetine inhibited the EEG changes caused by 4-aminopyridine for the ictal and postictal periods and increases in auditory brainstem responses in guinea pigs. The dose used for 4-aminopyridine and vinpocetine was 2 mg/kg. 20

Clinical data – The effect of Cavinton 15 to 45 mg/day on epilepsy was studied with different anticonvulsants. In 20 of the 31 patients treated with Cavinton , frequency of attacks significantly decreased or complete disappeared; 7 patients showed no improvement and 4 experienced deterioration. Cavinton was most effective in generalized tonic-clonic convulsions. 25

The effect of Cavinton in preventing neurologic disorders was studied in 61 newborns with hypoxic ischemic encephalopathy caused by intracranial birth trauma. Group 1 included 20 patients receiving conventional therapy; seizures disappeared in 6 patients. Group 2 included 41 patients given Cavinton ; seizures disappeared in 27 patients. Twenty-nine children were subsequently followed for 1 year. Convulsive paroxysms recurred in 4 patients in group 1. No convulsive syndrome was recorded for patients in group 2; these same patients also had a decrease in intracranial hypertension and normalization of psychomotor development. 26

Psychopharmacological effects
Clinical data

Vinpocetine, at increasing doses (30, 45, and 60 mg/day), was ineffective in improving cognitive deficits in 15 Alzheimer patients participating in a 1-year, double-blind, placebo-controlled, open-labeled pilot trial. 27

In a randomized, double-blind, crossover study, 12 women receiving either vinpocetine (10, 20, 40 mg) or placebo for 2 days completed a battery of psychological tests (critical flicker fusion, choice reaction time, subjective ratings of drug effects, and a Sternberg Memory Scanning Test) on day 3 of treatment, 1 hour after the morning dose of vinpocetine. Statistically significant changes in memory as assessed by the Sternberg Memory Scanning Test were observed with vinpocetine 40 mg compared with placebo. 28

Cavinton , when combined with protiadenum, improved psychopharmacotherapy of depressive disorders in patients with organic psychosyndromes. In a 16-week, placebo-controlled, randomized, double-blind, multicenter trial, 203 patients received vinpocetine 10 or 20 mg (3 times daily) or placebo (3 times daily). Primary outcomes were assessed from the Clinical Global Impression scale, using measurements from cognitive performance and quality of life. Side effects were comparable in treatment and placebo groups. Patients treated with vinpocetine reported statistically significant improvements in all tests. 29 , 30 , 31

Acute Ischemic Stroke
Animal data

Vinpocetine significantly decreased infarct volume (42%; P < 0.05) on permanent middle cerebral artery occlusion in rats compared with control; the neuroprotective potency of vinpocetine is compared with that of flunarizine or nimodipine. Vinpocetine also may reduce the development of atherosclerosis. In a 3-month study in rabbits given cholesterol-rich diets, 3 of 4 groups (4 rabbits in each group) fed vinpocetine supplements displayed decreased calcium content in various organ systems. 32 , 33

Clinical data

A reduction in red blood cell deformability is a contributory or risk factor for stroke. Vinpocetine, administered in a single oral dose of 10 mg, increased red blood cell deformability in 5 healthy men. When compared with single oral doses of pentoxifylline 300 mg and nicergoline 20 mg, vinpocetine was more effective in increasing red blood cell deformability. 34 , 35 , 36

The effect of a single-dose intravenous infusion of vinpocetine on cerebral blood flow and glucose metabolism was studied in poststroke patients. Results indicated that glucose transport (intracellular uptake and release) was affected in the whole brain, in the contralateral hemisphere, and in the peri-infarction area of the symptomatic hemisphere. Numerous studies document the effect of vinpocetine-modifying utilization of glucose in the brain (in acute ischemic and chronic stroke patients), particularly in the affected hemisphere. 37 , 38 , 39

A pilot, single-blind, randomized trial examined the effect of vinpocetine on 30 patients diagnosed with acute ischemic stroke who could be treated within 72 hours of stroke onset. Patients were randomly assigned to receive 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 vinpocetine-treated group scored only marginally better at 3 months follow-up ( P = 0.05, ANOVA). Patients did not report any adverse reactions. 40

The effect of vinpocetine on compromised cerebral blood perfusion and oxygenation in 43 patients with ischemic stroke was examined in a double-blind, randomized, placebo-controlled study. Patients received either a single dose of intravenous vinpocetine 20 mg in saline 500 mL or saline 500 mL alone as placebo. Results from transcranial Doppler and near infrared spectroscopy methods indicated increased cerebral perfusion and parenchymal oxygen extraction frontolaterally on the side of the lesion. 41

Chronic Cerebral Vascular Ischemia

Results from animal and human data postulate that the neuroprotective action of vinpocetine is associated with its effect on calcium- and calmodulin-dependent cyclic guanosine monophosphate-phosphodiesterase 1, voltage-operated calcium channels, glutamate receptors, and voltage-dependent sodium channels. 42 , 43 , 44

Clinical data

Eighty-one patients with chronic forms of cerebral ischemia were treated orally or parenterally with Cavinton . Patients reported reduction in subjective manifestations of the disease such as asthenic disturbances. The therapeutic effect ranged from 40 minutes to 6 hours with intravenous infusion. The authors concluded that Cavinton increased cardiac output and cerebral blood supply, and decreased peripheral resistance of the cerebral vessels. A similar study was completed in 38 patients with cerebral ischemia and atherosclerosis alone (n = 22) or hypertension (n = 16). Results for patients receiving Cavinton demonstrated decreased peripheral vascular resistance and tone of small and median vessels of the brain, increased cardiac output, and improved rheological properties of the blood (lower globular volume, viscosity, and hematocrit). A study involving 171 patients found the drug to be more effective in young to middle-aged patients versus elderly patients, perhaps because of the organic changes in cerebral vessels in the elderly. Vinpocetine effects on the rheological properties of blood have been documented in other studies, particularly with parenteral administration. 45 , 46 , 47 , 48

In a double-blind clinical trial, 42 patients with chronic vascular senile cerebral dysfunction received vinpocetine 10 mg 3 times daily for 30 days followed by 5 mg 3 times daily for 60 days. Placebo tablets were given to another 42 patients over 90 days. Evaluations of the effectiveness of treatment from the Clinical Global Impression scale, the Sandoz Clinical Assessment-Geriatric scale, and the Mini-Mental Status Questionnaire were consistently higher in patients receiving vinpocetine. No serious side effects were reported. 49


Follow the suggested manufacturers' guidelines. Most clinical studies used vinpocetine 10 mg 3 times daily orally or parenterally.


Avoid use during pregnancy and lactation because of lack of clinical studies.


Because vinpocetine decreases platelet aggregation, caution is warranted in patients receiving blood thinning agents. The effect of pretreatment with vinpocetine on prothrombin prolongation was studied in 18 men receiving warfarin 25 mg. A clinically important interaction was not demonstrated. 50 , 51

Drug/Food Interactions

In an open-label, crossover study, the bioavailability of vinpocetine was increased 60% to 100% when taken with food compared with fasting conditions. 52 , 53 , 54 , 55

Adverse Reactions

One review article reported flushing, rashes, and minor GI problems. 1


None well documented in the scientific literature. The drug is metabolized exclusively in the liver in dogs and humans. In rats, vinpocetine was widely distributed in lung, spleen, liver, and kidney tissues, and also was found in brain, heart, muscle, and blood. Both vinpocetine and apovincaminic acid are absorbed from the GI tract. Vinpocetine appears to follow linear pharmacokinetics. 56 , 57 , 58 , 59


1. Vinpocetine. Altern Med Rev . 2002;7:240-243.
2. Gulyás B, Halldin C, Vas A, et al. [ 11 C]Vinpocetine: a prospective peripheral benzodiazepine receptor ligand for primate PET studies. J Neurol Sci . 2005;219-223;229-230.
3. Kraus G, Schulz H, Lohmann A. Determination of apovincaminic acid in serum by means of high-performance liquid chromatography. J Chromatogr . 1992;573:323-327.
4. Karashurov S. The effect of kavinton on bronchial tonus in brachial asthma patients [in Russian]. Eksp Klin Farmakol . 1994;57:35-36.
5. Burtsev E, Savkov V, Shprakh V, Burtsev M. 10-year experience with using Cavinton in cerebrovascular disorders. Zh Nevropatol Psikhiatr Im S S Korsakova . 1992;92:56-60.
6. Karpati E, Biro K, Kukorelli T. Investigation of vasoactive agents with indole skeletons at Richter Ltd [in Hungarian]. Acta Pharm Hung . 2002;72:25-36.
7. Kiss B, Karpati E. Mechanism of action of vinpocetine [in Hungarian]. Acta Pharm Hung . 1996;66:213-224.
8. Olah VA, Balla G, Balla J, Szabolcs A, Karmazsin L. An in vitro study of the hydroxyl scavenger effect of Cavinton . Acta Paediatr Hung . 1990;30:309-316.
9. Pereira C, Agostinho P, Moreira P, Duarte A, Santos M, Oliveira C. Neuroprotection strategies: effect of Vinpocetine in vitro Oxidative Stress Models. Acta Med Port . 2003;16:401-406.
10. Horvath B, Marton Z, Halmosi R, et al. In vitro antioxidant properties of pentoxifylline, piracetam, and vinpocetine. Clin Neuropharmacol . 2002;25:37-42.
11. Santos M, Duarte A, Moreira P, Oliveira C. Synaptosomal response to oxidative stress: effect of vinpocetine. Free Radic Res . 2000;32:57-66.
12. Gabryel B, Adamek M, Pudelko A, Malecki A, Trzeciak H. Piracetam and vinpocetine exert cytoprotective activity and prevent apoptosis of astrocytes in vitro in hypoxia and reoxygenation. Neurotoxicology . 2002;23:19-31.
13. Kolarov G, Orbetsova M, Nalbanski B, et al. Complex effects of cavinton on climacteric symptoms. Akush Ginekol . 2001;42:37-41.
14. Kiss E. Adjuvant effect of cavinton in the treatment of climacteric symptoms. Ther Hung . 1990;38:170-173.
15. Nosalova V, Machova J, Babulova A. Protective action of vinpocetine against experimentally induced gastric damage in rats. Arzneimittelforschung . 1993;43:981-985.
16. Kovalev I, Baskakov M, Popov A, et al. Studying cGMP-dependent mechanisms of vinpocetine effect on smooth muscle cells [in Russian]. Eksp Klin Farmakol . 2003;66:25-28.
17. Phillips PG, Long L, Wilkins MR, Morrell NW. cAMP phosphodiesterase inhibitors potentiate effects of prostacyclin analogs in hypoxic pulmonary vascular remodeling. Am J Physiol Lung Cell Mol Physiol . 2005;288:L103-L105.
18. Truss M, Stief C, Uckert S, et al. Initial clinical experience with the selective phosphodiesterase-I isoenzyme inhibitor vinpocetine in the treatment of urge incontinence and low compliance bladder. World J Urol . 2000;18:439-443.
19. Truss M, Stief C, Uckert S, et al. Phosphodiesterase 1 inhibition in the treatment of lower urinary tract dysfunction: from bench to bedside. World J Urol . 2001;19:344-350.
20. Sitges M, Nekrassov V. Vinpocetine prevents 4-aminopyridine-induced changes in the EEG, the auditory brainstem responses and hearing. Clin Neurophysiol . 2004;115:2711-2717.
21. Maliavina US, Ovchinnikov IUM, Fasenko VP, Maliev BM, Kalinina MV, Dadasheva BB. Cavinton prevention of neurosensory hypoacousis in patients with different forms of tuberculosis [in Russian]. Vestn Otorinolaringol . 2003;(3):35-40.
22. Sitges M, Galvan E, Nekrassov V. Vinpocetine blockade of sodium channels inhibits the rise in sodium and calcium induced by 4-aminopyridine in synaptosomes. Neurochem Int . 2005;46:533-540.
23. Dutov AA, Tolpyshev BA, Karpov VN, Petrov AP. Effect of Cavinton on convulsions caused by chemical substances [in Russian]. Farmakol Toksikol . 1986;49:22-25.
24. Nekrassov V, Sitges M. Vinpocetine inhibits the epileptic cortical activity and auditory alterations induced by pentylenetetrazole in the guinea pig in vivo. Epilepsy Res . 2004;60:63-71.
25. Dutov AA, Tolpyshev BA, Petrov AP, Gladun VN. Use of cavinton in epilepsy [in Russian]. Zh Nevropatol Psikhiatr Im S S Korsakova . 1986;86:850-855.
26. Dutov AA, Gal'tvanitsa GA, Volkova VA, Sukhanova ON, Lavrishcheva TG, Petrov AP. Cavinton in the prevention of the convulsive syndrome in children after birth injury [in Russian]. Zh Nevropatol Psikhiatr Im S S Korsakova . 1991;91:21-22.
27. Thal LJ, Salmon DP, Lasker B, Bower D, Klauber MR. The safety and lack of efficacy of vinpocetine in Alzheimer's disease. J Am Geriatr Soc . 1989;37:515-520.
28. Subhan Z, Hindmarch I. Psychopharmacological effects of vinpocetine in normal healthy volunteers. Eur J Clin Pharmacol . 1985;28:567-571.
29. Otroshchenko N. Psychopharmacotherapy in combine treatment of depressive disorders in patients with brain pathology affected by the Chernobyl Atomic Electric Power Station accident [in Russian]. Lik Sprava . 2000;September:8-10.
30. Hindmarch I, Fuchs HH, Erzigkeit H. Efficacy and tolerance of vinpocetine in ambulant patients suffering from mild to moderate organic psychosyndromes. Int Clin Psychopharmacol . 1991;6:31-43.
31. Szatmari SZ, Whitehouse PJ. Vinpocetine for cognitive impairment and dementia. Cochrane Database Syst Rev . 2003;(1):CD003119.
32. Dezsi L, Kis-Varga I, Nagy J, Komlodi Z, Karpati E. Neuroprotective effects of vinpocetine in vivo and in vitro. Apovincaminic acid derivatives as potential therapeutic tools in ischemic stroke [in Hungarian]. Acta Pharm Hung . 2002;72:84-91.
33. Yasui M, Yano I, Ota K, Oshima A. Contents of calcium, phosphorus and aluminum in central nervous system, liver and kidney of rabbits with experimental atherosclerosis – scavenger effects of vinpocetine on the deposition of elements. No To Shinkei . 1990;42:325-331.
34. Hayakawa M. Effect of vinpocetine on red blood cell deformability in stroke patients. Arzneimittelforschung . 1992;42:425-427.
35. Hayakawa M. Effect of vinpocetine on red blood cell deformability in vivo measured by a new centrifugation method. Arzneimittelforschung . 1992;42:281-283.
36. Hayakawa M. Comparative efficacy of vinpocetine, pentoxifylline and nicergoline on red blood cell deformability. Arzneimittelforschung . 1992;42:108-110.
37. Gulyas B, Bonoczk P, Vas A, et al. The effect of a single-dose intravenous vinpocetine on brain metabolism in patients with ischemic stroke [in Hungarian]. Orv Hetil . 2001;March 4:142:443-449.
38. Feigin VL, Doronin BM, Popova TF, Gribatcheva EV, Tchervov DV. Vinpocetine treatment in acute ischaemic stroke: a pilot single-blind randomized clinical trial. Eur J Neurol . 2001;8:81-85.
39. Bonoczk P, Panczel G, Nagy Z. Vinpocetine increases cerebral blood flow and oxygenation in stroke patients: a near infrared spectroscopy and transcranial Doppler study. Eur J Ultrasound . 2002;15:85-91.
40. Szakall S, Boros I, Balkay L, et al. Cerebral effects of a single dose of intravenous vinpocetine in chronic stroke patients: a PET study. J Neuroimaging . 1998;8:197-204.
41. Szilagyi G, Nagy Z, Balkay L, et al. Effects of vinpocetine on the redistribution of cerebral blood flow and glucose metabolism in chronic ischemic stroke patients: a PET study. J Neurol Sci . 2005;229-230:275-284.
42. Erdo SL, Molnár P, Lakics V, Bence J, Tömösközi Z. Vincamine and vincanol are potent blockers of voltage-gated Na+ channels. Eur J Pharmacol . 1996;314:69-73.
43. Bonoczk P, Gulyas B, Adam-Vizi V, et al. Role of sodium channel inhibition in neuroprotection: effect of vinpocetine. Brain Res Bull . 2000;53:245-254.
44. Vas A, Gulyas B, Szabo Z, et al. Clinical and non-clinical investigations using positron emission tomography, near infrared spectroscopy and transcranial Doppler methods on the neuroprotective drug vinpocetine: a summary of evidences. J Neurol Sci . 2002;203-204:259-262.
45. Burtsev E, Tugutov A. Therapeutic effect of cavinton in chronic cerebral circulatory insufficiency. Zh Nevropatol Psikhiatr Im S S Korsakova . 1985;85:53-56.
46. Ishchenko M, Shkrobot S. Effect of cavinton on systemic and cerebral hemodynamics of patients with chronic cerebral circulatory insufficiency. Zh Nevropatol Psikhiatr Im S S Korsakova . 1985;85:1338-1342.
47. Szapary L, Horvath B, Alexy T, et al. Effect of vinpocetin on the hemorheologic parameters in patients with chronic cerebrovascular disease [in Hungarian]. Orv Hetil . 2003;144:973-978.
48. Burtsev E, Shprakh V, Savkov V. Effectiveness of using cavinton in patients of different ages with chronic forms of cerebrovascular diseases (clinico-rheographic research) [in Russian]. Zh Nevropatol Psikhiatr Im S S Korsakova . 1988;88:39-44.
49. Balestreri R, Fontana L, Astengo F. A double-blind placebo controlled evaluation of the safety and efficacy of vinpocetine in the treatment of patients with chronic vascular senile cerebral dysfunction. J Am Geriatr Soc . 1987;35:425-430.
50. Akopov SE, Gabrielian ES. Effects of aspirin, dipyridamole, nifedipine and cavinton which act on platelet aggregation induced by different aggregating agents alone and in combination. Eur J Clin Pharmacol . 1992;42:257-259.
51. Hitzenberger G, Sommer W, Grandt R. Influence of vinpocetine on warfarin-induced inhibition of coagulation. Int J Clin Pharmacol Ther Toxicol . 1990;28:323-328.
52. Lohmann A, Dingler E, Sommer W, Schaffler K, Wober W, Schmidt W. Bioavailability of vinpocetine and interference of the time of application with food intake. Arzneimittelforschung . 1992;42:914-917.
53. Bhatti JZ, Hindmarch I. Vinpocetine effects on cognitive impairments produced by flunitrazepam. Int Clin Psychopharmacol . 1987;2:325-331.
54. Hitzenberger G, Schmid R, Braun W, Grandt R. Vinpocetine therapy does not change imipramine pharmacokinetics in man. Int J Clin Pharmacol Ther Toxicol . 1990;28:99-104.
55. Molnar P, Erdo S. Vinpocetine is as potent as phenytoin to block voltage-gated Na+ channels in rat cortical neurons. Eur J Pharmacol . 1995;273:303-306.
56. Miskolczi P, Kozma K, Polgar M, Vereczkey L. Pharmacokinetics of vinpocetine and its main metabolite apovincaminic acid before and after the chronic oral administration of vinpocetine to humans. Eur J Drug Metab Pharmacokinet . 1990;15:1-5.
57. Pudleiner P, Vereczkey L. Study on the absorption of vinpocetine and apovincaminic acid. Eur J Drug Metab Pharmacokinet . 1993;18:317-321.
58. Yao JH, Su CY, Chu XY. Pharmacokinetics and disposition of vinpocetine in rats [in Chinese]. Yao Xue Xue Bao . 1994;29:81-85.
59. Szakacs T, Veres Z, Vereczkey L. In vitro-in vivo correlation of the pharmacokinetics of vinpocetine. Pol J Pharmacol . 2001;53:623-628.

Copyright © 2009 Wolters Kluwer Health