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(Stroke. 1972;3:268.)
© 1972 American Heart Association, Inc.

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The Course of Experimental Cerebral Infarction--The Development of Increased Intracranial Pressure

James H. Halsey JR. M.D.¹ Norman F. Capra B.S.¹

¹ Division of Neurology, Department of Medicine, the University of Alabama Medical Center, 1919 Seventh Avenue South, Birmingham, Alabama, 35233

In cats being subjected to surgical occlusion of the middle cerebral artery, regional oxygen availability (O₂a) was monitored continuously from four open-tip platinum electrodes in the ischemic hemisphere and one in the control hemisphere. Extradural pressure over the convexity of the ischemic hemisphere was measured hourly. The animals were killed 24 hours after occlusion. Ten animals developing substantial increases in extradural pressure as a consequence of cerebral infarction were compared with ten which did not. The two groups did not differ in severity of the initial ischemic insult resulting from the arterial ligation, in blood pressure following occlusion, or in hematocrit, P_COCO2, or oxygen saturation.

The most important difference between the two groups was in the course of regional O₂a in the ischemic hemispheres following occlusion. In the animals which ultimately developed increased intracranial pressure the recovery of regional O₂a was slower and less complete. After the ninth hour postocclusion O₂a declined progressively, clearly related to rising intracranial pressure. In the animals which developed increased extradural pressure, it rose progressively to a mean of 40 mm Hg by 24 hours postocclusion. The intracranial pressure changes during the first few hours seemed insufficient to account for the early failure of recovery of regional O₂a, unless they are viewed as averages which obscure important regional intracerebral pressure changes.

Key Words: oxygen availability • regional cerebral blood flow • P_COCO2

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