Document Detail

Twenty-four-hour heart preservation using continuous cold perfusion and copper (II) complexes.
MedLine Citation:
PMID:  9878309     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: During long-term in vitro heart preservation and subsequent reperfusion, irreversible tissue damage occurs in part due to reactive oxygen species. Therefore, inhibition of generation of oxygen-derived free radicals and the related oxidative damage of ischemic tissue may be useful in maintaining heart function after long-term preservation. Complexes of Cu(II) may cause disproportionation of superoxide and thus may function as an inhibitor of the effects of oxygen-derived free radicals. METHODS: In this study, 24-h preservation of isolated rat hearts was performed. Using the Langendorff technique, hearts were perfused for 24 h with a hypothermic, moderately hyperkalemic (15 mM KCl) solution containing various metabolic and membrane-stabilizing additives at constant low pressure. In addition, the potential benefit of the addition of two Cu(II) compounds (Cu(II) Cl2 and Cu(II)2Asp4) to the perfusion solution was examined. RESULTS: The Cu(II)Cl2-treated hearts were significantly better preserved than control hearts after 24 h of preservation with regard to recovery of systolic pressure, coronary flow, max +dP/dt, and max -dP/dt. Lipid peroxidation as estimated by myocardial malonaldehyde (both P < 0. 001) and myocardial creatine kinase release (both P < 0.05 vs control) were significantly reduced in the Cu(II)Cl2 and Cu(II)2Asp4 groups. Overall, Cu(II)Cl2 best preserved the heart after 24 h of cold preservation with respect to indices of functional recovery, whereas Cu(II)2Asp4 did not significantly improve functional recovery compared to control. CONCLUSION: Low-pressure, cold perfusion with an enhanced solution is a potential method to preserve donor hearts in preparation for transplantation. The beneficial effect of Cu(II)Cl2 was attributed to (i) SOD activity of the Cu2+ species and/or (ii) termination of chain carriers in the lipid peroxidations by aqueous Cu2+ and Cu+ species. The negation of some of the positive effects of Cu2+ species by the introduction of acetylsalicylate was tentatively assigned to potentiation of the Ca2+ modality for reperfusion injury.
F W Sellke; H W Richter; G Dunphy; M Azodi; D L Ely
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The Journal of surgical research     Volume:  80     ISSN:  0022-4804     ISO Abbreviation:  J. Surg. Res.     Publication Date:  1998 Dec 
Date Detail:
Created Date:  1999-01-28     Completed Date:  1999-01-28     Revised Date:  2010-03-24    
Medline Journal Info:
Nlm Unique ID:  0376340     Medline TA:  J Surg Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  171-6     Citation Subset:  IM    
Copyright Information:
Copyright 1998 Academic Press.
Department of Surgery, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachusetts, 02215, USA.
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MeSH Terms
Aspirin / analogs & derivatives
Cold Temperature
Creatine Kinase / metabolism
Heart* / physiology
Lipid Peroxidation
Malondialdehyde / metabolism
Myocardial Reperfusion Injury / metabolism,  prevention & control
Organ Preservation / methods*
Rats, Inbred SHR
Reactive Oxygen Species / metabolism
Superoxide Dismutase / metabolism
Time Factors
Ventricular Function, Left
Reg. No./Substance:
0/Antioxidants; 0/Reactive Oxygen Species; 0/Solutions; 23642-01-5/tetrakis-mu-acetylsalicylato-dicopper(II); 50-78-2/Aspirin; 542-78-9/Malondialdehyde; 7440-50-8/Copper; 7447-39-4/cupric chloride; EC Dismutase; EC Kinase

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