The following have been shown to be functions of vinpocetine in animal and clinical studies:
Regulates calcium-channel blocking activity and voltage-gated sodium channel blocking activity.
Inhibits the acetylcholine release evoked by excitatory amino acids and protects neurons against excitotoxicity.
Inhibits a cyclic GMP phosphodiesterase and this may enhance cyclic GMP concentrations in the vascular smooth muscle, which may lead to reduced resistance of cerebral vessels, therefore enhancing cerebral flow.
May have possible antioxidant activity equivalent to vitamin E, reducing neural damages in pathological situations.
Toxicity of vinpocetine has not been detected in either animals or humans.
Adverse reactions include nausea, dizziness, insomnia, drowsiness, dry mouth, transient hypotension, transient tachycardia, pressure-type headache and facial flushing. Slight reductions in systolic, diastolic blood pressure and blood glucose concentrations have been reported.
Pregnant and lactating women should avoid vinpocetine supplements.
Those with a history of allergic reactions or hypersensitivity reactions with other vinca alkaloids, such as vinblastine and vincristine, should avoid vinpocetine.
Individuals with hypotension or orthostatic hypotension may have slight reductions in systolic and diastolic blood pressure and should be monitored by a physician when using vinpocetine.
Vinpocetine may decrease effectiveness of warfarin [Coumadinâ], an anticoagulant agent. Avoiding this combination unless supervised by a physician or pharmacist is advised.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Ischaemic Stroke: Stroke is the third leading cause of death and one of the most important causes of long-term disability in most Western nations. Currently, recommendations for stroke are antiplatelet therapy and aspirin, otherwise there is no medical or surgical therapy that can be uniformly recommended for patients with acute ischaemic stroke. The synthetic derivative of apovincamine or vinpocetine may help with cerebral ischaemia.
In a study on 12 chronic stroke patients between the ages of 55 and 70 who were hospitalized for 3 days, patients received a MRI the first day, an intravenous infusion of 500 ml physiological solution [Salsolâ], followed by anatomic scanning tests the second day and finally 20 mg of vinpocetine dissolved in 500 ml Salsolâ intravenously the third day. The authors found that single-dose vinpocetine does not affect significantly regional or global metabolic rates of glucose. However, the treatment improved significantly the transport of glucose through the blood-brain barrier in the whole brain. Vinpocetine increases the peripheral vascular resistance in the symptomatic hemisphere, with special regard to the affected region (MCA territory). This results in blood redistribution at the advantage of the less affected brain tissue, thus supplying more blood to brain tissue with higher glucose uptake. 4
In a pilot, single-blind study, 30 patients with verified diagnosis of acute ishaemic stroke were given 3 g of low-molecular weight dextran in 250 ml of isotonic saline alone or in combination of 10 mg o.d. of vinpocetine for 5 to 7 days followed by oral vinpocetine for 30 days. A relative risk reduction of poor outcome at 3 months follow-up was 30%, as defined by the modified Barthel Index, and 60% as defined by the modified Rankin score. There were no significant adverse effects seen, and a full-scale randomized placebo-controlled double blind trial is warranted to address the issue of effectiveness of vinpocetine treatment in acute ischaemic stroke. 5
A review was written on all published and unpublished trials comparing vinpocetine to either placebo or another reference treatment for acute stroke. The treatment started no later than 14 days after stroke onset. Researchers found that only one trial fulfilled selection criteria for inclusion in the review and concluded that there is not enough evidence to determine whether vinpocetine does or does not decrease case fatality and dependency in acute stroke.6
Nootropic Effect: Vinpocetine is known to have significant antiamnesic activity. The beneficial effect of vinpocetine is often attributed to cerebral vasodilation and an increase in the concentration of cyclic nucleotides in blood vessel myoctes. There is evidence that indicates the mechanisms of vinpocetine action may also include its direct interaction with nervous cells. Vinpocetine may be able to protect neurons against Ca2+ induced death.
A study on isolated neurons of the left and right parietal ganglions of the land snail treated with vinpocetine showed its effects on different types of K+ currents. The data from the research suggested that modulation of different types of K+ currents in neuronal membranes may contribute partially to the nootropic effect of vinpocentine through the regulation of intracellular Ca2+ concentrations.7
Incontinence: Therapy for the most common types of urinary incontinence is mostly surgical or the use of muscarinergic receptor blockers. These drugs do not exert adequate tissue selectivity and there are side effects that lead to discontinuation of the therapy. By inhibiting phosphodiesterase (PDE)-1 isoenzyme, vinpocetine may assist in the regulation of porcine and human detrusor smooth muscle contractility.
Nineteen patients with urgency urge incontinence, detrusor instablities or low compliance bladder were given 5 mg of vinpocetine for 2 weeks and then 10 mg for another 2 weeks. In 11 out of 19 patients or 57.9%, clinical symptoms and or urodynamic parameters were improved. Overall, data indicated that there might be a role for the PDE-1 inhibitor vinpocetine in the treatment of detrusor instabilities, urge incontinence, and low compliance bladder for patients not responding to anticholinergic pharmacological intervention. 8
Oxidative Stress: Oxidative stress refers to the cytotoxic effects of reactive oxygen species such as hydroxyl radical, superoxide anion and hydrogen peroxide, which may attack cellular components, promoting neuronal degeneration. Antioxidant drugs, such as vinpocetine, may delay or minimize neurodegeneration.
A study evaluated whether vinpocetine can act as an antioxidant and prevent formation of reactive oxygen species and lipid peroxidation in rat brain synaptosomes. Vinpocetine was found to inhibit ascorbate/Fe2+-stimulated consumption of oxygen and thiobarbituric acid reactive substances accumulation, an indicator of lipid peroxidation, in a concentration-dependent manner. Authors concluded that the antioxidant effect of vinpocetine might enhance the protective role exerted by the drug in reducing neuronal damage in pathological situations. 9
The dietary supplement information contained on this site has been compiled from published sources thought to be reliable, but it cannot be guaranteed. Efforts have been made to assure this information is accurate and current. However, some of this information may be purported or outdated due to ongoing research or discoveries. The authors, editors and publishers cannot accept responsibility for errors or omissions or for any consequences from applications of the information in this site and make no warranty, expressed or implied, with respect to the contents herein.
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