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Modeling Stroke in Mice: Permanent Coagulation of the Distal Middle Cerebral Artery
Published on: July 31, 2014
Mouse model of microembolic stroke and reperfusion
D N Atochin1, J C Murciano, Y Gürsoy-Ozdemir
1Cardiovascular Research Center, Massachusetts General Hospital, Charlestown, Massachusetts 02129, USA.
Stroke
|July 17, 2004
Summary
This study demonstrates that endogenous tissue plasminogen activator (tPA) is crucial for dissolving cerebral microemboli and restoring blood flow, significantly limiting brain injury in a mouse stroke model.
Area of Science:
- Neuroscience
- Vascular Biology
- Thrombosis Research
Background:
- Stroke research often utilizes vessel occlusion models.
- A novel microembolic stroke model allows for controlled study of fibrinolysis.
- This model uses preformed fibrin microemboli susceptible to natural clot dissolution.
Purpose of the Study:
- To investigate the role of fibrinolysis in acute ischemic stroke.
- To establish and validate a mouse model of cerebral microembolism.
- To determine the contribution of endogenous tissue plasminogen activator (tPA) to stroke recovery.
Main Methods:
- Injection of calibrated fibrin microemboli into the mouse cerebral circulation.
- Assessment of microemboli distribution, cerebral blood flow, and neurological deficits.
- Comparison of wild-type mice with tissue plasminogen activator knockout (tPA-/-) mice.
Main Results:
- Microemboli induced dose-dependent brain injury and neurological deficits.
- Spontaneous reperfusion occurred with moderate microemboli doses, but injury persisted.
- tPA knockout significantly delayed emboli dissolution, blood flow restoration, and worsened brain infarction.
Conclusions:
- A reproducible mouse stroke model was developed using controlled microemboli dosage.
- This model allows for the investigation of spontaneous fibrinolysis, unlike vessel occlusion models.
- Endogenous tPA plays a critical role in resolving cerebral thrombosis and mitigating stroke damage.
