Remote ischemic preconditioning (RIPC), a brief transient episode of ischemia/reperfusion in distant tissues or organs, renders remote tissues and organs resistant to a subsequent prolonged ischemic insult.1 The RIPC stimulus may include occlusion of blood vessels in animal models, reduction of respired atmospheric oxygen intermittently before ischemia, or occlusion of the arteries of the arm by tourniquet.2 First described in a dog model of cardiac reperfusion in the 1980s, exposure to preclinical ischemic preconditioning involving the temporary occlusion of the coronary arteries restricted the myocardial injury caused by a subsequent sustained occlusion.3 Clinical outcomes in a number of ischemic conditions in humans have shown consistent improvement with RIPC, including decreased infarct size after myocardial infarction,4,5 slower progression of imaging lesions and cognitive decline in patients with cerebral small vessel disease,6 accelerated recovery from hypoxic ischemic brain injury after cardiac arrest,7 and reduced subsequent infarct volumes in patients with severe carotid stenosis undergoing carotid artery stenting.8 RIPC protects cells and tissue from future ischemia via a complex interplay of inflammatory, apoptotic, and neuroregenerative pathways that operate in parallel and in a complex manner.2,9 In the brain, RIPC primes nitric oxide formation, storage, and signaling and triggers synthesis of proapoptotic and antiapoptotic proteins such as B-cell lymphoma 2.2 It also stimulates neurogenesis and angiogenesis by upregulating brain-derived neurotropic factor and vascular endothelial growth factor production.2

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