The damaging effects of inflammation after prolonged myocardial ischemia are typically manifest during the period of reperfusion. The imbalance between free radical generation and availability of natural free radical scavengers during postischemic reperfusion set the stage for free radical injury. Calcium overload may convert reversible ischemic damage to fatal myocyte contracture. Complement activation and neutrophil activation, adhesion, and diapedesis are central components of the damaging inflammatory response. Cytokines such as tumor necrosis factor and IL1 simulate IL8 synthesis which is also a potent chemoattractant for neutrophils. The endothelial contribution to ischemic-reperfusion injury results from an imbalance between the production of naturally occurring vasodilators, such as prostacycline and nitric oxide, and vasoconstrictor products, such as endothelin, thromboxane A2, and angiotensin 2. Knowledge of these basic mechanisms has stimulated the formulation of preservation solutions and strategies to ameliorate the inflammatory response during reperfusion.