Maintenance of left ventricular function (90%) after twenty-four-hour heart preservation with deferoxamine.
During 24-h in vitro heart preservation and reperfusion, irreversible tissue damage occurs caused by reactive oxygen intermediates, such as superoxide radicals, singlet oxygen, hydrogen peroxide, hydroperoxyl, hydroxyl radicals, as well as the peroxynitrite radical. Reduction of the related oxidative damage of reperfused ischemic tissue by free radical scavengers and metal chelators is of primary importance in maintaining heart function. We assessed whether deferoxamine (DFR) added to a cardioplegia solution decreased free radical formation during 24-h cold (5 degrees C) heart preservation and normothermic reperfusion (37 degrees C) in the Langendorff isolated perfused rat heart. The deferoxamine treated hearts were significantly (p less than .001) better preserved than the control hearts after 24 h of preservation with regard to recovery of left ventricular diastolic pressure, contractility (+dP/dt), relaxation (-dP/dt), creatine kinase release, and lipid peroxidation. DFR preserved cell membrane integrity and maintained 93% of left ventricular contractility. The evidence suggests that DFR reduces lipid peroxidation damage by reducing free radical formation and thereby maintaining normal coronary perfusion flow and myocardial function.
Ely
D
D
Department of Biology, University of Akron, OH 44325.
Dunphy
G
G
Dollwet
H
H
Richter
H
H
Sellke
F
F
Azodi
M
M
D000818:Animals; D003402:Creatine Kinase / Q000187:drug effects; D003676:Deferoxamine / Q000494:pharmacology*; D003971:Diastole / Q000187:drug effects; D006321:Heart / Q000187:drug effects*; D066298:In Vitro Techniques; D008315:Malondialdehyde / Q000032:analysis; D009200:Myocardial Contraction / Q000187:drug effects; D015425:Myocardial Reperfusion; D009926:Organ Preservation; D051381:Rats; D011918:Rats, Inbred SHR; D016277:Ventricular Function, Left / Q000187:drug effects*
D008315:Malondialdehyde; D003402:Creatine Kinase; D003676:Deferoxamine