An experiment was planned to observe the histopathological alteration with administration of the Rheomacrodex and blood pressure changes in induced cerebral infarct after occlusion. Eighty well developed cats, weighing 2.3 to 3.5kg, were used in this experiment. The right MCA was exposed through temporal approach and the proximal part of the MCA was occluded with a silver clip. The animals were divided into 4 groups: The control group was comprised of 20 cats with occlusion of the right MCA alone, Rheomacrodex-treated group was comprised of 20 cats after occlusion of right MCA, induced hypotension and hypertension groups consisted in each 20 cats following occlusion of the MCA. The animals were sacrificed at intervals of 3 hours, 6 hours, 24 hours, 1 week and 2 weeks respectively after occlusion of the MCA. The animals were studied for clinical deficits and histopathological changes of the cerebral infarct according to the time courses. The results obtained were as follows: 1) In the control group, severe contralateral hemiplegia was developed in the early stage following the MCA occlusion, however the neurological deficits were progressively improved to the state of abnormal walking in 24 hours to 2 weeks. The hemorrhagic infarct was involving the basal ganglia, internal capsule and extending to the cortex with mild brain edema in the early stage and the area of the infarct was gradually enlarged from 6 hours to 24 hours following the MCA occlusion. Although the brain edema of surrounding area of the lesion was remained unchanged, the size and distribution of the infarct were decreased in one week to 2 weeks. Extensive ischemic neuronal damage was observed in the control group. 2) In the Rheomacrodex-treated group, mild to moderate neurological deficit was developed in the early stage after MCA occlusion and the deficit was less severe than control group. The clinical deficit was improving in the time course and one case had shown completely normal activity in 2 weeks. The distribution of the infarct was well defined and it was smaller than control group. The infarct mainly involved the basal ganglia and internal capsule. The area of the infarct was gradually enlarged from 6 hours to one week after MCA occlusion, then the extent of the infarct was decreased in 2 weeks. The ischemic neuronal change in this group was less severe than control group. 3) In the induced hypotension group, the early neurological deficit was worse than that of the control group and severe hemiplegia was developed in one week. There was minimal improvement of the neurological deficit in 2 weeks. The area of the infarct was ill-defined and hemorrhagic extending a large portion of the brain with severe brain edema. The infart was involving the basal ganglia, internal capsule, claustrum and the cortex from 3 hours to 24 hours after the occlusion and the area of the infarct was not changed during the observation. Severe ischemic nerve cell change or resolution of the cells was oserved in this group. 4) In the induced hypertension group, the neurological deficit was mild and it was better than that of the control group. The distribution of the infarct was well localized and minimum in extent. The extent of the infarct was not changed during the observation. There was no observable gross brain edema and the ischemic nerve cell changes were not severe.