Lidocaine Protects from Myocardial Damage due to Ischemia and Reperfusion in Mice by Its Antiapoptotic Effects

摘要: Background: Perioperative myocardial ischemia poses a vital threat to surgical patients. Means protect postischemic myocardium are clinically not available. Lidocaine has been demonstrated exert antiinflammatory pleiotropic effects. The authors set out test if lidocaine protects ischemic from reperfusion injury. Method: A mouse model of transient coronary artery ligation (30 min) and (24 h) was used with animal care committee approval. Infarct size area-at-risk were determined. Leukocyte recruitment quantified on immunohisto-chemical stainings. Apoptosis assessed using enzyme-linked immunosorbent assay detect histone modifications terminal deoxynucleotidyl transferase dUTP nick end labeling assays. effects leukocyte-endothelial interactions in vitro by parallel-plate flow chamber or static adhesion Results: per reduced 27% mice treated bolus (1 mg/kg) before continuous infusion (0.6 mg · kg -1 h ) during (P < 0.005). Neutrophil density the infarct periinfarct zone lidocaine, although infiltrated area was. Terminal labeling-positive cardiomyocytes endothelial cells significantly lidocaine. In vitro, no effect leukocyte rolling firm resting activated endothelium demonstrable. cardiomyocyte apoptosis induced hypoxia reoxygenation (3h/1h) significantly. likewise when administered after insult. Conclusion: exerts cardioprotective This is mediated through an antiapoptotic pathway may be therapeutically exploitable.