The development of ischemic cerebral edema was studied in terms of the intracranial hydrostatic factor. Adult mongrel cats underwent occlusion of the right middle cerebral artery via the transorbital approach to induce focal cerebral ischemia. Three hours after the arterial occlusion, hypertension was produced for 30 minutes. Based on the extent of the microcirculation derangement estimated from the regional cerebral blood flow (rCBF) and carbon filling assays, the brain was divided into three zones: the center of the ischemic zone, the periphery of the ischemic zone, and the nonischemic zone. Each zone was observed for changes in the rCBF, the water content of brain tissue, blood-brain barrier impairment, the architecture of the cerebral microvessels, and histology. Comparison of the hypertensive and normotensive groups revealed that the hypertensive animals underwent a progressive decrease in the rCBF in the peripheral ischemic zone after induction of hypertension, which became significant 6 hours after the production of cerebral ischemia. The water content of the peripheral ischemic zone in the hypertensive group was significantly higher than that of the normotensive group during the 6 hours following the induction of ischemia. Experimental hypertension caused a microcirculatory disturbance in the peripheral ischemic zone that steadily spread and worsened; within 24 hours of the induction of ischemia, brain edema progressed. It appears that focal brain edema, which developed in the periphery of the ischemic zone following the induction of transient hypertension and ischemia, grew progressively more severe and contributed to a secondary circulatory disturbance that resulted in global edema.