Table 1. Pathophysiologic Mechanisms of Myocardial I/R Injury.

■ Ion accumulation ○ Intracellular calcium overload ○ Increased intracellular sodium ○ Drop in pH with rapid normalization upon reperfusion ■ Dissipation of mitochondrial membrane potential ○ Mitochondrial permeability transition pore (mPTP) ■ Free radical formation/reactive oxygen species (ROS) ○ Generation from Xanthine oxidase ○ Release of reactive mitochondrial intermediates ○ Neutrophil infiltration ○ ROS-induced ROS ■ Dysregulated nitric oxide (NO) metabolism ○ Loss of NO-vasodilation ○ Accumulation of reactive peroxynitrite ■Apoptosis and autophagy ■ Endothelial dysfunction ○ Cytokine and chemokine signaling ○ Expression of cellular adhesion markers ○ Impaired vasodilation ■Platelet aggregation and microembolization ■ Immune activation ○ Innate immunity (e.g. complement activation, expression of Toll-like receptors) ○ Neutrophil accumulation ○ Cell-mediated damage (macrophage and T-cell)