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Bilateral Common Carotid Artery Occlusion as an Adequate Preconditioning Stimulus to Induce Early Ischemic Tolerance to Focal Cerebral Ischemia
Published on: May 9, 2013
Delayed tolerance with repetitive transient focal ischemic preconditioning in the mouse
Jian Zhang1, Zeng-Jin Yang, Judith A Klaus
1Department of Neurosurgery, Johns Hopkins University School of Medicine, 600 N. Wolfe Street, Blalock 1404, Baltimore, MD 21287, USA.
Stroke
|February 2, 2008
Summary
This study developed a mouse model for delayed ischemic tolerance using repetitive middle cerebral artery occlusion (MCAO). This method effectively reduced stroke severity and infarct volume without causing neuronal death.
Area of Science:
- Neuroscience
- Cerebrovascular Research
- Ischemic Stroke Models
Background:
- Transient ischemic attacks (TIAs) are stroke risk factors but may induce ischemic tolerance, potentially reducing stroke severity.
- Developing reliable models for studying ischemic tolerance is crucial for understanding stroke pathophysiology and developing neuroprotective strategies.
Purpose of the Study:
- To establish a mouse model of delayed ischemic tolerance using repetitive, transient middle cerebral artery occlusion (MCAO).
- To investigate the efficacy of this ischemic preconditioning (IPC) model in reducing infarct volume and neuronal damage.
Main Methods:
- Mice underwent ischemic preconditioning (IPC) involving repetitive MCAO episodes (2x5-minute or more severe) at 45-minute intervals.
- A 90-minute test MCAO was performed 24 to 96 hours post-IPC under halothane or isoflurane anesthesia.
- Infarct volumes and neuronal cell death were assessed 6 days after the test MCAO.
Main Results:
- IPC with 2x5-minute MCAO episodes induced maximal infarct reduction (striatum: 70%, cortex: 64%) at a 72-hour delay when using halothane anesthesia.
- Isoflurane anesthesia resulted in less prominent infarct reduction (striatum: 34%, cortex: 9%) compared to halothane.
- Increased IPC severity (3x5-minute or 1x15-minute MCAO) under isoflurane enhanced infarct reduction but also increased neuronal cell death.
Conclusions:
- Repetitive focal ischemic preconditioning (IPC) can be titrated to induce delayed tolerance in mouse striatum and cortex.
- This IPC model effectively reduces infarct volume without causing significant neuronal death when appropriately controlled.
- Anesthetic choice (halothane vs. isoflurane) significantly impacts the efficacy of IPC-induced delayed tolerance.
