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Departments of 1 Biology and 2 Chemistry, The University of Akron, Akron, Ohio 44325-3908; 3 BioPreserve Medical Corporation, Redmond, Washington 98052; and 4 Division of Cardiothoracic Surgery, Department of Medicine of Beth Israel-Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts 02215
During 24 h in vitro heart preservation and
reperfusion, tissue damage occurs that seriously reduces cardiac
function. Prevention of free radical production during preservation and
reperfusion of ischemic tissue using free radical scavengers is of
primary importance in maintaining optimal heart function in long-term preservation protocols. We examined whether mannitol (68 mM) and albumin (1.4 µM) in combination with other cardioplegia enhancers decreased free radical formation and edema and increased cardiac function during 24-h cold (5°C) heart preservation and warm
(37°C) reperfusion in the Langendorff-isolated rat heart. The
performance of mannitol-treated hearts was significantly decreased
compared with that of hearts without mannitol treatment after 24 h of
preservation with regard to recovery of diastolic pressure,
contractility (+dP/dt), relaxation
(
dP/dt), myocardial creatine
kinase release, coronary flow, and lipid peroxidation.
Albumin-treated hearts demonstrated higher cardiac function
(contractility and coronary flow especially) than hearts not treated
with albumin or hearts treated with mannitol, and this appears to be
due to the positive effects of increased cellular metabolism and the
enhancement of membrane stability.
organ preservation; free radicals; reperfusion injury; scavengers
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