Pashkovska N.V.
Bukovinian State Medical University, Chernivtsy,
Ukraine
ENDOTHELIAL
DYSFUNCTIONS IN PATIENTS WITH DIABETIC ENCEPHALOPATHY
The endothelium is a complex
organ with a multitude of properties essential for control of vascular
functions. It controls the tone of the underlying
vascular smooth muscle through the production of vasodilator mediators. The
endothelium-derived relaxing factors comprise nitric oxide, prostacyclin, and a
still elusive endothelium-derived hyperpolarizing factor [3].
Vascular endothelium
damage is known as
one of the major mechanisms in pathogenesis of chronic complications in diabetes
mellitus (DM). Factors associated with
endothelial dysfunction in diabetes
include activation of protein kinase C, overexpression of growth factors and/or
cytokines, and oxidative stress [4].
Encephalopathies of various genesis
tend to be the most important problem of present medicine. One of the leading causes of their development is DM. Diabetic encephalopathy (DE) is commonly considered to
be a variant of dyscirculatory encephalopathy. The pathogenesis is still
uncertain, but chronic hyperglycemia, vascular disease, repeated hypoglycemic
episodes, and possibly direct effects of insulin on the brain have been
implicated [1]. Nevertheless,
the degree of endothelial dysfunction in DE, haven’t been studied by other investigators in
dependence on the stage and type of basic disease.
The indices of circulating
desquamated endotheliocytes and endothelium-dependent vasodilatation (EDVD) of brachial artery were studied to
detect the degree of endothelial dysfunction in patients with DE in comparison with patients that
suffer from discirculatory encephalopathy of non-diabetic genesis.
The aim of
our study was to study differential peculiarities of EDVD in
patients with diabetic and non-diabetic encephalopathy.
The study group comprised 66 patients with vascular encephalopathy (32 with DE and 20 with non-diabetic encephalopathy). EDVD was evaluated according to
Celermayer-Sorensen’s test (EnVisor HD” (Philips, USA)) [2,
6]. The statistical evaluation was carried out by the t-test.
The study demonstrated, that dyscirculatory encephalopathy
was followed by reliably significant (Ð<0,001)
decrease of EDVD rate (5,6±0,21%) as compared
with controls (10,8±0,51%).
In case of DE the rate of EDVD was
more than two times decreased (4,9±0,23%) as compared
with control rate (Ð<0,001).
EDVD was more affected in type 2 DM (4,5±0,29%, Ð<0,05),
than in type 1 (5,5±0,31%), that indicated more severe
damage of vascular endothelium in case of non-insulin-dependent DM.
It
is necessary to mention, that changes of EDVD in DE were reliably more evident as compared with patients
suffering from non-diabetic dyscirculatory encephalopathy (6,4±0,29%).
This is explained, as we concluded,
by the direct toxic influence of increased glucose concentration on vascular endothelial
cells. This toxicity may lower the endothelium-dependent
vasodilatation, elevate the vasoconstriction, stimulate the hyperplasia of
smooth muscles cells, lead to vascular remodeling and development of
atherosclerosis.
The
endothelium is the thin layer of cells that line the interior surface of blood
vessels, forming an interface between circulating blood in the lumen and the
rest of the vessel wall. Endothelial cells line the entire circulatory system,
from the heart to the smallest capillary. These cells reduce friction of the
flow of blood allowing the fluid to be pumped further. Circulating endothelial
cells might be used as a surrogate non-invasive marker
for the study of vascular alterations.
The objectives of our study were to reveal the peculiarities of endothelial
dysfunction in patients with DE according to blood level of desquamated
endotheliocytes in dependence on the stage and type of DM. The estimation of endothelaemia was
carried out according to the method described previously [5].
The study concerned a group of 66
patients with DE (32 with type 1 DM and 34 with type 2 DM). Stage I DE was
diagnosed in 23 patients of studied group, stage II and III – in 25 and 18
patients respectively.
The findings
demonstrated, that endothelial desquamation was observed in the group of healthy
individuals as well as in the group of patients, suffering from DE.
In healthy
individuals blood level of desquamated endotheliocytes accounted 3,2±0,36·104/l.
In patients
with stage I DE this index reached 12,8±0,64·104/l, stage
Consequently,
the progression of DE was followed by proportional
augmentation of the blood
concentration of desquamated endothelioin
cytes. The index of endotheliocytemia was reliably higher in type 2 DM as
compared with type 1 diabetics (Ð<0,05), that
indicated more significant implication of vascular endothelium damages in the pathogenesis of non-insulin-dependent
DM. The role of endothelial dysfunction in type 2 diabetes is more complicated
than that for type 1. The effects of aging, hyperlipidemia, hypertension, and
other factors add to the complexity of the problem.
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