Stroke, Vol 19, 1544-1549, Copyright © 1988 by American Heart Association
M Kudo and T Nagayama
Using light and electron microscopy, we studied the interaction between
lipids and host tissue for up to 15 days after experimentally produced
cerebral infarcts in 16 rats. A lipid-dense zone was formed along the
periphery of the infarcts before a glial response started; a glycogen- rich
zone appeared peripheral to the lipid zone. Macrophages and astrocytes then
started to proliferate in the lipid and glycogen-rich zones. The cerebral
tissue within the lipid zone underwent complete necrosis.
Ultrastructurally, lipids were observed in the edematous areas as well as
in various types of hematogenous and resident cells. Glycogen granules were
present mainly in the astrocytic processes. Macrophages rapidly evolved
into foamy macrophages in the central necrotic areas, whereas foamy
transformation was not striking in the peripheral, less injured areas.
Reactive fibrous astrocytes also contained varying amounts of lipids. The
exact biologic significance of the lipid zone in the premacrophagic stage
remains unclear; however, since lipids are hydrophobic, they may function
as a barrier against edema fluid extension into the adjacent tissue.
ARTICLES
Light and electron microscopic study of lipid accumulation along margins of experimental cerebral infarcts in rats
Department of Pathology, Toho University School of Medicine, Tokyo, Japan.
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