Recent studies have demonstrated that ischemic preconditioning prevents reperfusion-induced endothelial dysfunction. However, the question of the influence of preconditioning on the occurrence of the no-reflow phenomenon remains open. The receptor mechanisms of the cardioprotective and vasoprotective effects of preconditioning are different. The ability of preconditioning to prevent reperfusion-induced endothelial dysfunction is associated with activation of bradykinin B2 receptors and is independent of stimulation of adenosine receptors. The vasoprotective effect of preconditioning is mediated by mechanisms associated with activation of protein kinase C, NO synthase, and cyclooxygenase, the opening of mitochondrial KATP channels, and increases in the antioxidant defense of the heart. Delayed preconditioning also has an endothelium-protecting effect. Triggers for these effects are NO •, O2 •, and peroxynitrite, and endothelial NO synthase may be the end effector is.
- endothelial NO synthase
- no-reflow phenomenon
- reperfusion-induced endothelial dysfunction
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