Vinpocetine (VP) is a selective inhibitor of Ca++ calmodulin-dependent
cGMP phosphodiesterase (PDE). It is assumed that this inhibition enhances
intracellular cGMP levels in vascular smooth muscles leading to reduced
resistance of cerebral blood. This in turn, will lead to neuroprotection
in transient ischemic attacks (TIAs).
The aim of the present study was to investigate the effect of VP on
some peripheral menoamines in human namely, serum norepinephrine
(NE) and blood serotonin (5HT). Moreover, cortical NE, 5-HT and dopamine
(DA) were investigated in the cortex of brain rat subjected to experimental
transient ischemia induced by carotid artery occlusion.
Regarding the clinical part, it was carried out on forty (40) individuals.
Ten (10) of them were volunteers, above 40 years old, both sexes and of
good health as controls. The other thirty (30) were outpatients from Benha
university hospitals, both sexes (22 males and 8 females), aged from 40-
60 years (mean 51+1.1) and were suffering from TLAs. They entered the
study according to definite inclusive and exclusive criteria, and divided
into 2 groups each of them was 15 patients. The first group did not take
medications (Non-Vinpocetine Treated Group), and the other group treated
with VP (5mg td.$) for 2 months. Results of this part revealed signfficant
elevation (P<0.05) of peripheral serum NE and blood 5 HT in Tills nontreated
patients compared to the control group, and this level is main-
tamed elevated significantly in VP treated patients compared to control
group, however, this elevation was not significant compared to TIAs nontreated
group (P<0.05).
In the experimental part of ow- work, we used 126 albino rats, both
sexes, weighing from 150-200 gms and divided into three groups (I), (11)
and (III) each group consisted of 42 rats. Six rats from each group were
served for determination of cerebral (schemia using triphenyl tetrazoliurn
chloride (T.T.C) (subgroup. d). The other 36 rats in each group were subdivided
into 3 sub-groups (a), (19) and (c) each consisted of 12 rats, and
were used for determination of cortical NE, 5HT and DA respectively.
Group (1) did not receive any medication and served as control group.
Group (II) subjected to transient ischemia by occlusion of carotid arteries.
Group (III) treated with VP (5 pg/kg/B.W., 1.P.) ten minutes before induction
of ischemia. Results of this part revealed significant elevation of NE
5I11' and DA in the cortex of ischemic rats Group (II) compared to control
group (I) (P<0.05) and the level of 511T is maintained elevated significantly
in group (117) compared to control group (I) or ischemic non-treated group
(II) while the level of DA and NE were reduced significantly (P<0.05) In
group (III) treated with VP before ischemia compared t9 group (1) or group
In conclusion, the protective effect of VP in TIAs may have an adding
mechanism attributed to maintaining elevated level of serum NE, blood 5
HT and also due to reduced level of cortical DA and NE and maintained
elevated level of 5PIT.
|
