Endothelial cell toxicity of solid-organ preservation solutions

Endothelial cell damage caused by myocardial cardioplegic solutions (Bretschneider HTK and St. Thomas' Hospital No. 2) or renal and hepatic cold storage solutions (modified Collins and University of Wisconsin solution) was assessed in monolayer cultures of adult human venous endothelial cells at 4 ° to 10 °C with phase-contrast microscopy. St. Thomas' Hospital solution caused the cells to contract, resulting in disruption of monolayer integrity and opening of intercellular gaps, and resulted in a 24-hour postexposure survival of 51.0% ± 2.4%. Bretschneider HTK solution altered cellular morphology less and produced the best postexposure survival (80.2% ± 2.6%; p < 0.001). Although morphology was altered the least with University of Wisconsin solution, postex-posure survival with this solution, which was similar to that with modified Collins solution, was superior to that with St. Thomas' (p < 0.01) but inferior to that with Bretschneider HTK (p < 0.05). The superior protection provided by Bretschneider HTK was due to its additives histidine, tryptophan, and KH-2-oxygluterate (p < 0.005), and to its low chloride content (p < 0.005). Furthermore, modifying St. Thomas' solution by decreasing its chloride content improved cell survival to 71.2% ± 2.3% (p < 0.001). Normothermic (37 °C) exposure to Bretschneider HTK, modified Collins, and University of Wisconsin solution was cytotoxic, whereas normothermic exposure to St. Thomas' cardioplegia was not. In conclusion, the preservation solution that is the least harmful to endothelial cells at hypothermia is Bretschneider HTK cardioplegic solution. © 1990.