Biomedical Engineering Reference
In-Depth Information
We review data concerning adhesion molecules and brain infarction,
summarizing the results of important i ndings including those from animal studies
for the acute phage and summarizing the i ndings of studies on the association
between brain infarction and endothelial dysfunction in large and small vessels
level for the chronic phage. Importance is being attached to the involvement of
leukocytes at the capillary level as a cause of the no-rel ow phenomenon at er
brain ischemia and reperfusion.
In clinical trials on the use of anti-intercellular
adhesion molecule 1 (ICAM-1) antibody in the acute phase, no signii cant ef ect
has been observed and no progress has been made in the clinical application
of anti-adhesion molecule therapy targeting leukocytes. At the chronic phage,
there is thought to be repeated ischemia and reperfusion in microvessels in the
area surrounding the ischemia focus, and it has been suggested that there is the
association between endothelial dysfunction and the development and progression
of SVD with lacunar infarction and white matter lesions. It is therefore necessary to
study the usefulness of antiplatelet and antihypertensive agents having protection
of the vessel endothelium.
Endothelial dysfunction in microvessels is thought to play an important role
in the pathogenesis of SVD and its progression. h ere is therefore a need to study
therapeutic strategies targeting vascular endothelial cells in more detail.
INTRODUCTION
Brain ischemia induces expression of inl ammatory mediators in vascular
endothelial cells, which causes adhesion molecules to be expressed on them, and
enhances interaction between leukocytes and the endothelial cells. Frijns and
Kappelle (2002) reviewed the association between leukocyte-endothelial cell and
adhesion molecules in ischemic cerebrovascular disease. Although endothelial
dysfunction may play an important role in the progression of brain ischemia in
large and small vessels, the pathogenesis dif ers in vascular bed levels. In particular,
the pathogenesis of brain infarction in small and microvessels is still unclear. It
is necessary to target therapy on the vascular endothelium in order to prevent
the development and progression of ischemic stroke. In this chapter, we primarily
discuss the association between brain infarction and microcirculation dysfunction
with small-vessel disease (SVD) at the acute and chronic phage.
ADHESION MOLECULES (AMs) IN ACUTE BRAIN
INFARCTION
AM Expression Associated with Brain Ischemia and
Reperfusion
In brain infarction, stimulation by various cytokines and endotoxins enhances
AM expression, which increases coagulation activation, leukocyte accumulation
