Stroke, Vol 7, 547-554, Copyright © 1976 by American Heart Association
L Symon, NM Branston and AJ Strong
The autoregulatory capacity of areas of the cerebral circulation subjected
to ischemia by acute middle cerebral occlusion has been assessed in
experimental primates. Autoregulation was tested to a rise in blood
pressure induced by aramine, and to a fall in blood pressure induced by
exsanguination. Whole hemisphere autoregulation was substantially disturbed
due to both increased blood pressure and lowered blood pressure, but
fractionation of this response indicated that autoregulation to increased
blood pressure was preserved in the parasagittal and intermediate zones of
the hemisphere, and totally lost in the region of the sylvian opercula
where middle cerebral occlusion had produced the most dense ischemia. In
relation to reduced perfusion pressure, autoregulation was again widely
impaired and assessment of the degree of impairment by areas indicated no
significant difference between the areas of the sylvian opercula and the
remainder of the lateral aspect of the hemisphere studied. Where the degree
of ischemia in each individual electrode was assessed, however, it appeared
that the degree of auto-regulatory loss to decreased perfusion pressure was
dependent upon the intensity of ischemia, and autoregulation was partially
preserved in electrodes whose immediate post-occulsion flow values were
greater than 40% of basal flow. Retransfusion following exsanguination in
animals with acute middle cerebral occlusion indicated that there was a
linear relationship between the degreee of reperfusion achieved by
retransfusion and the intensity of ischemia induced by exsanguination
following middle cerebral occlusion. Thus there was some support for the
no-reflow phenomenon in intensely ischemic areas.
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