Endothelial activation--a strategic event during postischemic myocardial inflammation

Reperfusion after limited ischemia increases leukocyte adhesion, which may contribute to postischemic myocardial and endothelial stunning. Leukocyte adhesion is enhanced immediately after the onset of reperfusion, indicating rapid regulatory mechanisms. In addition, de novo synthesis of, e.g., adhesion molecules induced by reperfusion has been described, providing a prolonged postischemic inflammatory reaction. Enhanced transcription of adhesion molecules involves NF kappa B activation which appears as an essential transcription factor for reperfusion-induced subacute endothelial activation. Both, acute and subacute endothelial activation seem to contribute to the final extent of leukocyte-dependent reperfusion injury and successive treatment of both appears to be a promising therapeutic strategy for postischemic myocardial inflammation and its detrimental effects.