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2. [Preconditioning impact on coronary perfusion during ischemia and reperfusion of heart].

Author

Maslov LN, Lishmanov IuB, Oeltgen P, Peĭ JM, Krylatov AV, Barzakh EI, Portnichenko AG, and Meshoulam R

Subjects
Bradykinin metabolism, Endothelium, Vascular metabolism, Enzyme Activation, Free Radicals metabolism, Humans, Myocardial Reperfusion Injury metabolism, Myocardial Reperfusion Injury physiopathology, Nitric Oxide metabolism, Potassium Channels metabolism, Prostaglandin-Endoperoxide Synthases metabolism, Protein Kinase C metabolism, Receptors, Purinergic P1 metabolism, Endothelium, Vascular physiopathology, Heart physiopathology, Ischemic Preconditioning, Myocardial, Myocardial Reperfusion Injury prevention & control, Nitric Oxide Synthase Type III metabolism, Receptor, Bradykinin B2 metabolism
Abstract

Recent studies have confirmed that ischemic preconditioning prevents appearance of reperfusion endothelial dysfunction. However, the issue of preconditioning impact on no-reflow phenomenon remains unresolved. The receptor mechanisms involved in the cardioprotective and vasoprotective effects of preconditioning are different. The ability of preconditioning in preventing reperfusion endothelial dysfunction is dependent upon bradykinin B2-receptor activation and not dependent upon adenosine receptor stimulation. The vasoprotective effect of preconditioning is mediated via mechanisms relying in part on activation of protein kinase C, NO-synthase, cyclooxygenase, mitochondrial K(ATP)-channel opening and an enhancement of antioxidative protection of the heart. The delayed preconditioning also exerts endothelium-protective effect. Peroxynitrite, NO* and O2* are the triggers of this effect but a possible end-effector involves endothelial NO-synthase.

Published
2012

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