Primate Model of Cerebral Hematoma

Abstract

Using specific anesthetic agents, permanent segmental occlusion of the proximal middle cerebral artery (MCA) causes ischemic infarction limited to the putamen and other deep hemispheral structures in primates. Using this model, 25 rhesus monkeys were subjected to acute arterial hypertension before, during and up to 5 days after onset of MCA occlusion in order to reevaluate the possible role of the ischemic process in pathogenesis of cerebral hemorrhage. Norepinephrine infusion induced prompt rapid rise in mean arterial pressure (MAP) and intracranial pressure (ICP) limited to the duration of infusion. This procedure produced acute ischemic lesions which were totally bland but topographically more extensive than untreated controls; in chronic lesions, however, deep nuclear masses showed hemorrhagic infarction. Animals given 5% CO₂ in air had slowly progressive elevation in ICP and MAP. Acute specimens showed intact, widely-dilated vessels surrounding the ischemic zones but without extravasations; when hypercarbia was induced 5 days after MCA occlusion, animals developed intracerebral hematomas involving putamen, external capsule and claustrum, occasionally dissecting through to ipsilateral ventricle. In acute cerebral ischemia, elevated MAP produced only quantitative changes in lesion size. In the vasoproliferative stages of mature infarction, MAP elevation induced by a cerebral vasoconstrictor caused hemorrhagic infarctions while cerebral vasodilation caused intracerebral hematomas.