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Vol. 297, Issue 2, 474-478, May 2001
Departments of Neurology (K.N., T.M.D., V.L.D.), Neuroscience
(T.M.D., V.L.D.), and Physiology (V.L.D.), Johns Hopkins University
School of Medicine, Baltimore, Maryland
Preconditioning to ischemic tolerance is a phenomenon in which brief
episodes of a subtoxic insult induce a robust protection against
the deleterious effects of subsequent, prolonged, lethal ischemia. The
subtoxic stimuli that constitute the preconditioning event are quite
diverse, ranging from brief ischemic episodes, spreading depression or
potassium depolarization, chemical inhibition of oxidative
phosphorylation, exposure to excitotoxins and cytokines. The beneficial
effects of preconditioning were first demonstrated in the heart; it is
now clear that preconditioning can induce ischemic tolerance in a
variety of organ systems including brain, heart, liver, small
intestine, skeletal muscle, kidney, and lung. There are two temporally
and mechanistically distinct types of protection afforded by
preconditioning stimuli, acute and delayed preconditioning. The
signaling cascades that initiate the acute and delayed
preconditioning responses may have similar biochemical components. However, the protective effects of acute preconditioning are protein synthesis-independent, mediated by post-translational protein modifications, and are short-lived. The effects of delayed preconditioning require new protein synthesis and are sustained for
days to weeks. Elucidation of the molecular mechanisms that are
involved in preconditioning and ischemic tolerance and identification of drugs that mimic this protective response have the potential to
improve the prognosis of patients at risk for ischemic injury. This
article focuses on recent findings on the effects of ischemic preconditioning in the cardiac and nervous systems and discusses potential targets for a successful therapeutic approach to limit ischemia-reperfusion injury.
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