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Cellular Injury During Ischemia
Edema Formation
 Ischemic
brain edema is a combination of two major types of edema:
cytotoxic (cellular) and vasogenic [Fishman RA. Cerebrospinal
Fluid in Diseases in the Nervous System. 2nd Ed. Philadelphia,
PA: W.B. Saunders Co; 1992:103-155]. Cytotoxic
edema evolves over minutes to hours and may be reversible,
while the vasogenic phase occurs over hours to days, and is
considered an irreversibly damaging process.
Cytotoxic edema is characterized by swelling
of all the cellular elements of the brain (shown). In
the presence of acute cerebral ischemia, neurons, glia (indicated
by astrocytes), and endothelial cells swell within minutes
of hypoxia due to failure of ATP-dependent ion (sodium and
calcium) transport. With the rapid accumulation of sodium
within cells, water follows to maintain osmotic equilibrium.
Increased intracellular calcium activates phospholipases and
the release of arachidonic acid, leading to the release of
oxygen-derived free radicals and infarction.
Vasogenic edema (not shown) is characterized
by an increase in extracellular fluid volume due to increased
permeability of brain capillary endothelial cells to macromolecular
serum proteins (e.g., albumin). Normally, the entry
of plasma protein-containing fluid into the extracellular
space is limited by tight endothelial cell junctions, but
in the presence of massive injury there is increased permeability
of brain capillary endothelial cells to large molecules.
Vasogenic edema can displace the brain hemisphere and, when
severe, lead to cerebral herniation.
Acute hypoxia initially causes cytotoxic edema,
followed within the next hours to days by the development
of vasogenic edema as infarction develops (Fishman, 1992).
The delayed onset of vasogenic edema suggests that time is
needed for the defects in endothelial cell function and permeability
to develop.
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