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 risein 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 remainderof 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 autoregulatory loss to decreased perfusion pressure was dependent upon the intensity of ischemia, and autoregulation was partially preserved in electrodes whose immediate post-occlusion flow values were greater than 40% of basal Row, but absent in electrodes whose flow values were less than 20% of basal flow. Retransfusion following exsanguination in animals with acute middle cerebral occlusion indicated that there was a linear relationship betweenthe degree 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.