Prolonged cold storage using a new histidine-tryptophan-ketoglutarate-based preservation solution in isogeneic cardiac mouse grafts.

ABSTRACT

AIMS: The aim of this study was to evaluate a new histidine-tryptophan-ketoglutarate (HTK)-based cold preservation solution in comparison with traditional HTK solution in a mouse cardiac transplant model and to assess the impact of chloride ions and of iron chelators. METHODS AND RESULTS: After 24 h cold ischaemia, traditional HTK-preserved hearts survived up to 13 days (4.4 ± 1.7 days; n = 8)). Hearts stored in the new solution without iron chelators (N46) showed significantly prolonged survival up to 2 months (N46 11.9 ± 8.7 days; P < 0.01; n = 7) and with iron chelators (DesfLK) up to 3 months (N46 DesfLK 12.7 ± 13.7 days; n = 6). Re-beating time was significantly shorter with the new solution (HTK 14.5 ± 5.9 min, N46 9.2 ± 2.7 min, N46 DesfLK 7.1 ± 3.7 min; P < 0.01). The new solution showed significantly decreased release of creatine kinase (HTK 25998 ± 8471 U/L, N46 13829 ± 7679 U/L, N46 DesfLK 3093 ± 597 U/L; P < 0.01 and n = 7 each) and lactate dehydrogenase (HTK 5391 ± 1062 U/L, N46 3428 ± 1890 U/L, P < 0.05; N46 DesfLK 682 ± 344 U/L, P < 0.01) and decreased histological evidence of injury. A chloride-poor variant of the new solution showed inferior graft survival. CONCLUSION: The new solution markedly attenuates myocardial injury and yields better graft survival than traditional HTK solution. The presence of chloride ions is crucial for heart preservation. Some protective effects are obviously caused by iron chelators.