Stroke, Vol 20, 641-645, Copyright © 1989 by American Heart Association
L Persson, HG Hardemark, HG Bolander, L Hillered and Y Olsson
Focal cerebral ischemia was produced in 45 rats by occlusion of the left
middle cerebral artery. Groups of rats were investigated over a long period
after occlusion, that is, from a few hours to 42 days after the production
of focal ischemia. Light microscopy showed infarcts in the frontoparietal
cortex and the lateral caudoputamen. The ischemic changes closely resembled
those found in ischemic infarcts in humans and followed a similar pattern
over time. Measurements of the sizes of the infarct, the ipsilateral
(operated) hemisphere, and the contralateral hemisphere from camera lucida
drawings revealed that the infarct size changed with time after occlusion.
Rats killed during the first 7 days (acute phase) had the largest infarcts;
in rats killed thereafter, the infarct size diminished. The size of the
ipsilateral hemisphere also changed with time; during the first 7 days
after occlusion this hemisphere was swollen and larger than the
contralateral hemisphere. We suggest that these acute changes are caused by
cerebral edema. After the first 7 days, enlargement of the ipsilateral
hemisphere gave way to a significant reduction in the size of both the
ipsilateral hemisphere and the infarct. We believe that the major reasons
for this shift in size are resorption of fluid together with diminished
production of edema and elimination of dead cells by macrophages. We
suggest that the amount of tissue loss (i.e., the degree of atrophy and the
remaining infarct "scar") found 21-42 days after occlusion (during the late
phase) is a measure of the total amount of tissue that succumbed as a
consequence of ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)
ARTICLES
Neurologic and neuropathologic outcome after middle cerebral artery occlusion in rats
Department of Neurosurgery, University of Uppsala, Sweden.
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