Role of sodium channel
inhibition in neuroprotection: effect of vinpocetine.
Bonoczk P, Gulyas B, Adam-Vizi V, Nemes A, Karpati E, Kiss B,
Kapas M, Szantay C, Koncz I, Zelles T, Vas A.
Chemical Works of Gedeon Richter
Ltd., Budapest, Hungary
Brain Res Bull 2000 Oct;53(3):245-54
Vinpocetine (ethyl apovincaminate)
discovered during the late 1960s has successfully been used in the treatment
of central nervous system disorders of cerebrovascular origin for decades. The
increase in the regional cerebral blood flow in response to vinpocetine
administration is well established and strengthened by new diagnostical
techniques (transcranial Doppler, near infrared spectroscopy, positron
emission tomography). The latest in vitro studies have revealed the effect of
the compound on Ca(2+)/calmodulin dependent cyclic guanosine
monophosphate-phosphodiesterase 1, voltage-operated Ca(2+) channels, glutamate
receptors and voltage dependent Na(+)-channels; the latest being especially
relevant to the neuroprotective action of vinpocetine. The good brain
penetration profile and heterogenous brain distribution pattern (mainly in the
thalamus, basal ganglia and visual cortex) of labelled vinpocetin were
demonstrated by positron emission tomography in primates and man.
Multicentric, randomized, placebo-controlled clinical studies proved the
efficacy of orally administered vinpocetin in patients with organic
psychosyndrome. Recently positron emission tomography studies have proved
that vinpocetine is able to redistribute regional cerebral blood flow and
enhance glucose supply of brain tissue in ischemic post-stroke patients.