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Acute microvascular platelet aggregation after subarachnoid hemorrhage.
Fatima A Sehba1, Gulam Mostafa, Victor Friedrich
1Department of Neurosurgery, Mount Sinai School of Medicine, New York, New York 10029-6574, USA. fatima.sehba@mssm.edu
Journal of Neurosurgery
|July 21, 2005
Summary
Platelet aggregates rapidly form in the brain
Area of Science:
- Neuroscience
- Hematology
- Cerebrovascular Research
Background:
- Acute cerebral ischemia mechanisms post-subarachnoid hemorrhage (SAH) are unclear.
- Platelet aggregation in major cerebral vessels after SAH is known, but microvascular involvement is unstudied.
- Microvascular platelet aggregates may obstruct blood flow and cause vessel injury.
Purpose of the Study:
- To investigate the hypothesis that platelets aggregate within the cerebral microvasculature acutely after SAH.
Main Methods:
- Subarachnoid hemorrhage (SAH) induced in rats via endovascular perforation.
- Immunostaining for glycoprotein (GP)IIb/IIIa to detect platelet aggregation at various time points post-SAH (10 minutes to 48 hours).
- Comparison with sham-operated control animals.
Main Results:
- Abundant GPIIb/IIIa-immunoreactive platelet aggregates detected in cerebral microvasculature 10 minutes post-SAH.
- Aggregate numbers decreased between 1–6 hours, then increased to a peak at 24 hours.
- No aggregates observed 48 hours post-SAH.
Conclusions:
- Widespread platelet aggregation occurs rapidly after SAH, with dynamic changes over 24 hours.
- Microvascular platelet aggregates are a potential contributor to reduced cerebral blood flow and ischemic injury post-SAH.