Conclusion And Future Directions

Induced tolerance to ischemia is an attractive strategy for preemptive neuroprotection in patients at high risk for cerebral ischemia in the near future. The mechanisms of preconditioning-acquired ischemic tolerance have not yet been completely characterized. Rapid preconditioning probably involves changes in membrane excitability and mitochondrial function, whereas delayed preconditioning probably involves multiple signaling pathways that activate a set of transcription factors and turn on a set of genes that define a new cellular phenotype that is characterized by increased resilience to ischemic stress. More work is needed to identify relevant molecules and therapeutic targets in the core of this pathway. Mediators of inflammation and pluripo-tent molecules, such as EETs, are potential targets for such future efforts. Until more specific and efficient inducers of endogenous tolerance are developed, pharmacologic preconditioning might be a feasible alternative for selected patients.

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