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Diabetes 53:454-462, 2004
© 2004 by the American Diabetes Association, Inc.

Absence of Inducible Nitric Oxide Synthase Reduces Myocardial Damage During Ischemia Reperfusion in Streptozotocin-Induced Hyperglycemic Mice

Raffaele Marfella1,2, Clara Di Filippo2,3, Katherine Esposito1,4, Francesco Nappo1, Elena Piegari3, Salvatore Cuzzocrea4, Liberato Berrino2,3, Francesco Rossi2,3, Dario Giugliano1,2, and Michele D’Amico2,3

1 Department of Geriatrics and Metabolic Diseases, Second University of Naples, Naples, Italy
2 "Centro di Eccellenza Cardiovascolare," Second University of Naples, Naples, Italy
3 Department of Experimental Medicine, Second University of Naples, Naples, Italy
4 Department of Pharmacology, University of Messina, Messina, Italy

We investigated the role of inducible nitric oxide synthase (iNOS) on ischemic myocardial damage and angiogenic process in genetically deficient iNOS (iNOS-/-) mice and wild-type littermates (iNOS+/+), with and without streptozotocin-induced (70 mg/kg intravenously) diabetes. After ischemia (25 min) and reperfusion (120 min), both iNOS+/+ and iNOS-/- diabetic mice (blood glucose 22 mmol/l) had myocardial infarct size greater than their respective nondiabetic littermates (P < 0.01). Myocardial infarct size (P < 0.05), apoptotic index (P < 0.005), and tissue levels of tumor necrosis factor (P < 0.01), interleukin-6 (P < 0.01), and interleukin-18 (P < 0.01) were higher in nondiabetic iNOS-/- mice compared with nondiabetic iNOS+/+ mice. As compared with diabetic iNOS-/- mice, diabetic iNOS+/+ mice showed a greater infarct size (P < 0.01) associated with the highest tissue levels of nitrotyrosine and proinflammatory cytokines, as well as apoptosis. The beneficial role of iNOS in modulating defensive responses against ischemia/reperfusion injury seems to be abolished in diabetic mice.

Address correspondence and reprint requests to Raffaele Marfella, Via Emilio Scaglione 141, 80145 Napoli, Italy. E-mail: raffaele.marfella{at}unina2.it


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Copyright © 2004 by the American Diabetes Association.