Cavinton Forte Mechanism of Action

Antihypoxydotic.
Pharmacology: Cavinton increases cerebral metabolism. It increases the glucose and oxygen consumption and utilization of the cerebral tissue, improves cerebral hypoxia tolerance; shifts glucose metabolism to the energetically more favourable aerobic pathway, but it increases the anaerobic pathway as well, by the inhibition of phosphodiesterase enzyme and by the stimulation of adenylate cyclase; it elevates the CAMP level of the brain; it elevates the ATP concentration and the ATP/AMP ratio in the brain and elevates the cerebral norepinephrine, dopamine and serotonin levels.
Cavinton considerably improves cerebral microcirculation. It inhibits platelet aggregation, reduces the pathologically increased blood viscosity, increases erythrocyte deformability and inhibits their adenosine uptake; it promotes oxygen transport into the tissues by reducing the oxygen affinity of erythrocytes.
Cavinton selectively and intensely increases cerebral blood flow and the share of the brain in cardiac output; it reduces cerebral vascular resistance without affecting systemic circulation (blood pressure, heart rate, cardiac output, total peripheral resistance); it does not elicit "steal phenomenon", on the contrary, it primarily improves the blood supply of the injured ischaemic area while it remains unchanged in the intact areas (inverse steal effect); it further increases blood flow which is already increased as a result of hypoxia.
Mechanisms of Action: Vinpocetine appears to have several different mechanisms of action that allow for its antioxidant, vasodilating and neuroprotective activities.
Voltage-Dependent Sodium Channel Inhibition: It has been hypothesized that vinpocetine's application in ischemic stroke is secondary to its effect on voltage-dependent sodium channels in the brain. Inhibition of sodium channels in neural tissue is the primary mechanism of several different drugs reported to have neuroprotective effects in experimental ischemia. This action, effectively blocking accumulation of sodium in neurons, decreases the damage of reperfusion injury and may be beneficial in lessening the toxic effects of oxidative stress resulting from anoxia.
Phosphodiesterase-1 Inhibition: Vinpocetine inhibits Ca⁺²/calmodulin-dependent phosphodiesterase (PDE) type 1. This effect would theoretically lead to an increase of cyclic AMP over cyclic GMP and may be responsible for the benefits in cerebral circulation and decreased platelet aggregation observed after vinpocetine administration.
Antioxidant Effects: Like vitamin E, vinpocetine is an effective scavenger of hydroxyl radicals. It has also been shown to inhibit lipid peroxidation in synaptosomes of murine brain tissue and to protect against global anoxia and hypoxia in animals. Vinpocetine has decreased areas of neuronal necrosis in animal models up to 60% in experimentally-induced ischemia.
Other Neuroprotective Effects: Vinpocetine has been shown to protect neurons from the toxicity of glutamate and N-methyl-d-aspartate (NMDA). Vinpocetine lowers blood viscosity in patients with cerebrovascular disease, has significant vasodilating properties, decreases platelet aggregation, and increases and maintains erythrocyte flexibility under oxidative stress, all of which are potentially beneficial in cerebrovascular disease. Vinpocetine causes a selective increase in cerebral blood flow and increases cerebral metabolic rate.
Pharmacokinetics: Vinpocetine, when taken on an empty stomach, has an absorption rate of 6.7%. When taken with food, absorption increases 60-100%. Vinpocetine reaches the bloodstream approximately 1 hr after administration, whether taken with food or on an empty stomach. The elimination half-life of the oral form is 1-2 hrs and the majority of vinpocetine is eliminated from the body within 8 hrs.
Recent studies, either following IV infusion of vinpocetine in patients with cerebrovascular disorders or using positron emission tomography (PET) scans in animals, have shown that vinpocetine crosses the blood-brain barrier and is taken up by cerebral tissue. PET studies have also clearly shown in human subjects, vinpocetine is preferentially absorbed in the central nervous system at twice the level that would be expected according to total body distribution. The highest uptake of vinpocetine was seen in the thalamus, putamen and neocortical regions.