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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