Introduction

The ability to withstand, respond to, and cope with ongoing stress is a fundamental property of all living organisms. At the cellular level, a stress response can be elicited by noxious agents, such as endotoxin and oxygen free radicals, and by disturbances in normal cellular and organ homeostasis, such as those occurring during ischemia and heat stress. When excessive, such stimuli can cause irreversible tissue damage. However, in several organs, including heart and brain, it has been shown that mild stress, including mild ischemic stress, may serve a beneficial role, by rapidly mobilizing existing defense mechanisms to cope with ongoing stress and by inducing a more delayed genomic response to cope with imminent threat. This phenomenon is generally referred to as preconditioning or tolerance, and rapid and delayed responses define 2 pathophysiologically distinct phases of tolerance, referred to as early or acute and delayed or late preconditioning (1). Ischemic preconditioning in brain is of particular importance because brain cells, particularly neurons, are critically dependent on oxygen and nutrients, and the slightest disruption of blood flow can irreversibly damage neurons and lead to permanent functional disability. Unfortunately, despite decades of research, clinically available treatment options for patients who experience cerebral ischemia are still limited. In this chapter, we review the efforts focused on determining endogenous mechanisms of protection that result from ischemic preconditioning and on efforts to translate mechanisms of tolerance into potential stroke therapies.

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