Abstract
Postischemic reperfusion causes microvascular endothelial cell dysfunction characterized by low shear stress, excessive oxidative stress and a reduced nitric oxide (NO) release. Recent studies have demonstrated that reduced shear forces are responsible for the impairment of endothelium-dependent vasodilation after ischemia reperfusion (I/R) injury. Preconditioning is an endogenous phenomenon whereby intermittent periods of ischemia provide protection against subsequent periods of I/R. Several models show that intermittent hypoxia (IH, brief periods of systemic hypoxia and reoxygenation), treatment with erythropoietin (EPO) and ultrasound exposure are methods of preconditioning. This chapter explores the hypothesis that these procedures that improve tolerance to subsequent I/R are directly related to shear stress. It acts as a biochemical mechanotransducer by modulating the production of vasoactive substances by endothelial cells. The adaptation of endothelial cells to high shear stress during the preconditioning period is crucial to ensure vasodilation and capillary perfusion during subsequent periods of I/R. Both IH and EPO treatment increase blood viscosity thus increasing shear stress associated with a reduced oxidative stress during postischemic reperfusion. Ultrasound treatment can also improve tolerance to I/R and normale shear stress during postischemic reperfusion by pulsatile mechanism acting on endothelial cells.
Keywords: Ischemic preconditioning, ischemia-reperfusion, shear stress, intermittent hypoxia, EPO, low intensity ultrasound
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