Myocardial reperfusion injury in neuronal nitric oxide synthase deficient mice

Background A substantial amount of data suggesting that endothelial cell ni tric oxide synthase (eNOS) plays a cardioprotective role in animal models o f ischemia-reperfusion injury has amassed. We have previously demonstrated that eNOS-deficient (-/-) mice exhibit significantly larger myocardial infa rcts than do wild-type mice. Few investigations have examined the neuronal form of nitric oxide synthase in the heart. The two constitutive isoforms h ave been demonstrated to play differing roles in studies of cerebral ischem ia-reperfusion, Objective To characterize the role of neuronal nitric oxide synthase (nNOS) in myocardial ischemia-reperfusion injury, Methods Wild-type and nNOS -/- mice were subjected to 20 min of coronary ar tery occlusion and 120 min of reflow. Results We found no significant difference between the two groups in terms of infarct size, Microscopic cross-sections from both groups were examined for infiltration of polymorphonuclear leukocyte, Hearts of nNOS -/-mice exh ibited significantly (P< 0.05) more polymorphonuclear leukocytes than did h earts of wild-type mice. Conclusion Despite the fact that eNOS plays a cardioprotective role in the ischemic-reperfused myocardium, we observed no change in size of myocardial infarcts when nNOS was genetically disrupted, Coron Artery Dis 11:593-597 (C) 2000 Lippincott Williams & Wilkins.