Mechanisms Of Ischemic Tolerance

Similar to what has been initially described in heart, ischemic tolerance in brain is biphasic, where tolerance is acquired shortly after the stimulus and at a delayed time point following preconditioning. Early tolerance against subsequent cerebral ischemia starts as early as 30 min after the preconditioning ischemic episode and lasts for approximately 2 hr (rapid preconditioning) (38,39). A second window of tolerance is observed 24 hr later, which lasts for 2 to 7 days (delayed preconditioning) (3,30,31). Early and delayed phases of tolerance represent 2 distinct responses to preconditioning, with different temporal profiles and mechanisms of protection. Acute preconditioning results from rapid changes in activity and posttranslational modifications of existing proteins, whereas delayed tolerance involves gene induction and de novo protein synthesis (40). Mechanistically, the early phase of preconditioning is usually attributed to flow-mediated mechanisms or changes in cellular metabolism, whereas delayed tolerance to ischemia represents a long-term, adaptive response to stress and genetic reprogramming in brain toward a more protected phenotype.

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