Biomedical Engineering Reference
In-Depth Information
found signii cantly impaired l ow-mediated vasodilation vs the control only in
lacunar infarction (Chen
et al.
2006). h e above studies indicate that awareness
of the involvement of endothelial dysfunction is important to understanding the
pathogenesis of SVD and, in the future, with respect to brain infarction subtypes
at the acute phase, it will be necessary to conduct intervention studies with drugs
having protection of the vessel endothelium such as phosphodiesterase inhibitors
like dipyridamol and cilostazol and HMG-CoA inhibitors (statins).
ADHESION MOLECULES IN CHRONIC BRAIN
INFARCTION
Carotid Atherosclerosis
To further clarify associations between chronic cerebral thrombosis and AMs,
investigations should target both large and small blood vessels. However, few
studies have been done on the latter. Regarding large blood vessels, in the past
many studies have noted an association with carotid artery plaque or carotid artery
stenosis, while an association between carotid artery stenosis and AMs is still
controversial. DeGraba
et al.
(1998) reported that ICAM-1 expression was greater
in symptomatic plaques than in asymptomatic plaques and that, for symptomatic
plaques, ICAM-1 expression was more enhanced in the high-grade region than
it was in the low-grade region. Also, the results of the Atherosclerosis Risk In
Communities (ARIC) study indicated that the relationship between ICAM-1 and
E-selectin and carotid artery atherosclerosis was independent of other traditional
risk factors (Hwang
et al.
1997). Another study showed that levels of sE-selectin and
sP-selectin were signii cantly elevated in patients who had previously symptomatic
carotid stenosis, though sICAM-1 and sVCAM-1 were not elevated. In contrast,
it was also reported that symptomatic carotid disease was not associated with
increased expression of AMs in the endothelium of advanced carotid plaques.
Cerebral Small-Vessel Disease (SVD)
At the chronic phage, brain ischemia and reperfusion is repeated in microvessels in
the region of the ischemic focus and the inducing factor of endothelial dysfunction
is likely to lead to development of small infarcts and progression of white matter
lesions (WMLs). Fassbender
et al.
(1999) reported that serum concentrations of
sE-selectin and sICAM-1 were signii cantly increased in patients with extracranial
and intracranial large-vessel disease and patients with cerebral SVD. h ese results
indicated that inl ammatory endothelial activation and adhesion of leukocytes
play similarly important roles in cerebral large- and small-vessel disease. Chronic
hyperglycemia and obesity with insulin resistance have been seen to reduce eNOS
