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SPORT SCIENTIST
Banned
This sounds like a safe drug to use when cutting, what do you think? Has anyone ever used it?
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.
Vinpocetine is a new cerebral metabolic activator which can improve cerebral circulation and enhance oxygen and glucose utilisation in the brain. Vinpocetine diminishes or reduces disturbances due to hypoxia or to deficient cerebral metabolism. Vinpocetine produces improvement in mental and neurological symptoms which are sequelae to cerebral haemorrhage, cerebral infarction (particularly multi- infarct) and cerebrosclerosis. Cerebral circulation is particularly enhanced in response to low oxygen levels in the brain and thus increased blood flow to the brain is not accompanied by reduced peripheral blood flow and side effects associated with that as hypertension. Vinpocetine improves oxygen and glucose utilisation by brain cells and increases their resistance to damage by hypoxia.
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.
THE INTERESTING BIT: SEE STUDY BELOW
Vinpocetine preferentially antagonizes quisqualate/AMPA receptor responses: evidence from release and ligand binding studies.
Kiss B, Cai NS, Erdo SL.
Pharmacological Research Centre, Gedeon Richter Ltd., Budapest, Hungary.
The effect of vinpocetine on excitatory amino acid receptors was examined in the rat brain by two different biochemical approaches. In release experiments with striatal slices, vinpocetine reduced the efflux of dopamine and acetylcholine evoked by glutamate, quisqualate and N-methyl-D-aspartate (NMDA), but not that evoked by kainate. In binding experiments with cortical membranes, vinpocetine reduced the binding of [3H]2-amino-3-3-hydroxy-s-methylisoxasole-4-yl-propionic acid ([3H]AMPA), a quisqualate partial agonist, in an incomplete manner, but failed to influence the binding of [3H]kainate and [3H]3-(2-carboxypyperazine-4-yl)-propyl-1-phosphonic acid ([3H]CPP), an NMDA agonist. These findings suggest that vinpocetine is a quisqualate/AMPA antagonist of some specificity and selectivity.
-BASICALLY IT REDUCES THE AMOUNT OF DOPAMINE/ACETYLCHOLINE LEAVING THE BRAIN, SUGGESTING A STRONG AMPHETAMINE-LIKE EFFECT.
SIDE EFFECTS:
Numerous clinical studies indicated that vinpocetine is safe during long-term administration. No serious side effects related to the treatment have been found (Balestreri et al., 1987; Kis, 1990; Feigin et al., 2001).
Szobor and Klein, (1976) established that vinpocetine (10-30 mg daily at combined oral and i.m. administration, or 30-45 mg daily orallly) did not change laboratory tests, blood pictures, blood sugar, liver functions, did not cumulate and did not produce allergic symptoms).
There are few reports about side effects of vinpocetine after i.v. administration. Some patients had a passing sensation of warmth after injection of the drug (Orosz et al., 1976; Hajiev and Yancheva, 1976; Ribári et al., 1976)
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.
Vinpocetine is a new cerebral metabolic activator which can improve cerebral circulation and enhance oxygen and glucose utilisation in the brain. Vinpocetine diminishes or reduces disturbances due to hypoxia or to deficient cerebral metabolism. Vinpocetine produces improvement in mental and neurological symptoms which are sequelae to cerebral haemorrhage, cerebral infarction (particularly multi- infarct) and cerebrosclerosis. Cerebral circulation is particularly enhanced in response to low oxygen levels in the brain and thus increased blood flow to the brain is not accompanied by reduced peripheral blood flow and side effects associated with that as hypertension. Vinpocetine improves oxygen and glucose utilisation by brain cells and increases their resistance to damage by hypoxia.
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.
THE INTERESTING BIT: SEE STUDY BELOW
Vinpocetine preferentially antagonizes quisqualate/AMPA receptor responses: evidence from release and ligand binding studies.
Kiss B, Cai NS, Erdo SL.
Pharmacological Research Centre, Gedeon Richter Ltd., Budapest, Hungary.
The effect of vinpocetine on excitatory amino acid receptors was examined in the rat brain by two different biochemical approaches. In release experiments with striatal slices, vinpocetine reduced the efflux of dopamine and acetylcholine evoked by glutamate, quisqualate and N-methyl-D-aspartate (NMDA), but not that evoked by kainate. In binding experiments with cortical membranes, vinpocetine reduced the binding of [3H]2-amino-3-3-hydroxy-s-methylisoxasole-4-yl-propionic acid ([3H]AMPA), a quisqualate partial agonist, in an incomplete manner, but failed to influence the binding of [3H]kainate and [3H]3-(2-carboxypyperazine-4-yl)-propyl-1-phosphonic acid ([3H]CPP), an NMDA agonist. These findings suggest that vinpocetine is a quisqualate/AMPA antagonist of some specificity and selectivity.
-BASICALLY IT REDUCES THE AMOUNT OF DOPAMINE/ACETYLCHOLINE LEAVING THE BRAIN, SUGGESTING A STRONG AMPHETAMINE-LIKE EFFECT.
SIDE EFFECTS:
Numerous clinical studies indicated that vinpocetine is safe during long-term administration. No serious side effects related to the treatment have been found (Balestreri et al., 1987; Kis, 1990; Feigin et al., 2001).
Szobor and Klein, (1976) established that vinpocetine (10-30 mg daily at combined oral and i.m. administration, or 30-45 mg daily orallly) did not change laboratory tests, blood pictures, blood sugar, liver functions, did not cumulate and did not produce allergic symptoms).
There are few reports about side effects of vinpocetine after i.v. administration. Some patients had a passing sensation of warmth after injection of the drug (Orosz et al., 1976; Hajiev and Yancheva, 1976; Ribári et al., 1976)
