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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 air had slowly progressive elevation in ICP and MAP. Acute specimens showed intact, widely-dilan hypercarbia was induced 5 days after MCA occlusion, animals developed intracerebral hematoma involving putamen, external capsule and claustrum, occasionally dissecting through to ipsilateral ventricle. In acute cerebral ischemia, elevated MAP produced only quantiative 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.
Insights
This study investigated how blood pressure affects stroke outcomes in primates. Elevated blood pressure during acute ischemic stroke led to larger lesions, while later elevations caused hemorrhagic transformations or hematomas.
Area of Science:
- Neuroscience
- Neurology
- Pathology
Background:
- Middle cerebral artery (MCA) occlusion in primates creates ischemic lesions in deep hemispheral structures.
- The role of ischemic processes and arterial hypertension in cerebral hemorrhage pathogenesis requires further investigation.
Purpose of the Study:
- To reevaluate the role of ischemic processes in cerebral hemorrhage pathogenesis.
- To investigate the effects of acute arterial hypertension on ischemic stroke lesions in a primate model.
Main Methods:
- Permanent segmental occlusion of the proximal MCA in 25 rhesus monkeys.
- Induction of acute arterial hypertension using norepinephrine infusion or hypercarbia (5% CO2 air).
- Evaluation of lesion development and characteristics at different time points post-MCA occlusion.
Main Results:
- Acute hypertension before/during MCA occlusion resulted in larger, bland ischemic lesions.
- Chronic lesions in animals subjected to hypertension showed hemorrhagic infarction.
- Hypercarbia-induced hypertension 5 days post-MCA occlusion led to intracerebral hematomas.
- Elevated mean arterial pressure (MAP) in acute ischemia only increased lesion size.
- MAP elevation with vasoconstrictors in mature infarction caused hemorrhagic infarctions; vasodilation caused hematomas.
Conclusions:
- Arterial hypertension can exacerbate acute ischemic lesions.
- The timing and nature of blood pressure changes significantly influence stroke outcomes, potentially leading to hemorrhagic transformation or hematoma formation.