Stroke, Vol 14, 22-27, Copyright © 1983 by American Heart Association
G Mies, LM Auer, G Ebhardt, H Traupe and WD Heiss
In 6 cats, cerebral infarction was produced by transorbital occlusion of
the left middle cerebral artery (MCA). Five animals developed typical
cortical infarcts. Eight weeks later, cerebral blood flow (CBF) was
determined by 14C-iodoantipyrine autoradiography and the number of intact
neurons was counted histologically. Two non-operated cats served as
controls. Cortical blood flow in the infarcted hemisphere was reduced by
24.6-74.4% when compared to the flow in the contralateral cortex and in
controls. Averaged white matter flow was decreased by 39.1%. Regional
cortical flow was gradually reduced from parasagittal regions towards the
infarct. In the surrounding of the infarct, cortical perfusion was
decreased to 24.8 +/- 9.7 ml/100 g/min, i.e. 19.7% of contralateral flow.
Although the infarcts were sharply demarcated macroscopically, the number
of cortical neurons decreased gradually from the midline to the
peri-infarct zone. A significant linear correlation was found between
absolute CBF-values and the number of neurons in areas of the infarcted
hemisphere. The homolateral gyrus lateralis had normal neuronal density but
flow was reduced by 20%. These findings suggest that the blood flow
reduction in tissue surrounding chronic infarcts is due to neuronal cell
loss and to functional inactivation caused by damage of afferent fibers.
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Flow and neuronal density in tissue surrounding chronic infarction
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