vinpocetine is chemically related to, and derived from vincamine, an alkaloid found in the periwinkle plant. Vinpocetine was introduced into clinical practice in europe more than two decades ago for its role in cerebrovascular disorders and related symptoms. Experiments with vinpocetine indicate that it can dilate blood vessels, enhance circulation in the brain, improve oxygen utilization, make red blood cells more pliable, and inhibit aggregation of platelets. Vinpocetine even has antioxidant properties. Levels peak in the bloodstream within an hour and a half after ingestion. Vinpocetine easily crosses the blood-brain barrier.

Introduction of vinpocetine

ethyl apovincaminate (vinpocetine) is a vincamine derivative has been used in the clinical practice for over 25 years for the treatment of cerebrovascular disorders and related symptoms. The effects of vinpocetine on cerebral blood flow, brain metabolism, memory functions, and its neuroprotective action have been confirmed in the past years in numerous animal experiments and human studies.
The aim of the present paper is to review the preclinical and clinical studies on vinpocetine.

Pharmacological properties of vinpocetine

vinpocetine exerts a brain neuroprotective effect by a combined action on cerebral circulation, brain metabolism, and rheological properties of the blood. Kiss and karpat summarized the pharmacological studies on vinpocetine. Early experiments showed an improvement of the cerebral circulation and oxygen utilization without changes in systemic circulation, cerebral protection in conditions of hypoxia/ischaemia, cognition-enhancing and anticonvulsant activity, and improvement of rheological properties of the blood. Later studies confirmed the above effects and clearly demonstrated a direct neuroprotective action at a cellular level.


Cerebral circulation

· increases brain perfusion by improvement of cerebral blood flow and decrease of the cerebral vascular resistance
· increases the cerebral capillary flow rate
· improves total cerebral blood flow in normal conditions and in hypoxic hypoxia

brain metabolism


· enhances the cerebral metabolic rate of oxygen
· prevents the local cerebral glucose utilization increase, caused by forebrain ischaemia of 10-min duration in rats
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