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  • Title: Deferoxamine, the newly developed iron chelator LK-614 and N-alpha-acetyl-histidine in myocardial protection.
    Author: Koch A, Loganathan S, Radovits T, Sack FU, Karck M, Szabó GB.
    Journal: Interact Cardiovasc Thorac Surg; 2010 Feb; 10(2):181-4. PubMed ID: 19914924.
    Abstract:
    During cold storage of donor hearts, reactive oxygen species produced by intracellular redox-active chelatable iron potentially alter myocardial function. To reduce this cold-induced injury we investigated the efficacy of two new modifications of the well established histidine-tryptophan-ketogluterate (HTK) solution (Custodiol) with the addition of N-alpha-acetyl-l-histidine and iron-chelators in a heterotopic rat heart transplantation model. The donor hearts were cardioplegically arrested with 20 ml cardioplegia and stored for 1 h. Then the hearts were anastomosed to the abdominal aorta and vena cava of the recipient (n=30). After 1 h reperfusion, myocardial function and energy charge potential were measured in three groups: HTK-1: addition of l-arginine and N-alpha-acetyl-l-histidine; HTK-2: addition of iron-chelators deferoxamine and LK-614; traditional HTK - control. After 1 h reperfusion, left ventricular systolic pressure (106+/-33 vs. 60+/-39, vs. 67+/-8 mmHg, P<0.05) and dP/dt minimal (-1388+/-627 vs. -660+/-446, vs. 871+/-188 mmHg/s, P<0.05) were significantly higher in the HTK-1 group. Energy charge potentials were not significantly different. This study showed that the novel modified HTK-1 solution improves myocardial contractility and relaxation after heart transplantation. Nevertheless, addition of the iron-chelators deferoxamine and LK-614 diminished these beneficial effects.
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