Nonesterified Fatty Acid Content of Rabbit Kidney Cortex Slices after Warm Ischemia and Low Temperature Preservation

Abstract

Nonesterified fatty acid content (NEFA) of rabbit kidney cortex slices preserved at low temperature after warm ischemia was examined. Kidney tissue slices were subjected to 60 min of warm (37°C) ischemia induced by anoxic gaseous phase incubation and then either had reperfusion simulated by normothermic oxygenated aqueous incubation or were preserved at 5°C up to 18 h with UW sodium gluconate solution and then reincubated at normothermia. Slice NEFA content increased during ischemia and remained significantly higher than controls during simulated reperfusion. Ischemic tissue slice NEFA content was significantly reduced by both 3- and 18-h preservations. There was a significant increase in NEFA content in 3-h preserved slices during simulated reperfusion. This increase was relatively unaffected by the addition of KCN to the incubation medium, suggesting that mitochondrial injury was induced by ultrashort preservation of ischemic tissue slices. Ischemic tissue slices preserved for 18 h increased in NEFA content during simulated reperfusion but did not appear more damaged than slices subjected to ischemia alone. Addition of quinacrine (100 μmol/l) to the cold preservation solution significantly reduced NEFA content during simulated reperfusion of slices preserved both 3 and 18 h with a greater effect in 18-h preserved slices. Quinacrine had no effect when added only during simulated reperfusion. KCN addition during simulated reperfusion indicated that quinacrine acted as a mitochondrial protectant in the absence of phospholipase inhibition under these conditions. This study showed that cold preservation may be useful for resuscitation of ischemic tissues harvested for transplantation. Treatments administered during cold preservation of ischemic tissue can have a lasting beneficial effect during reperfusion and may be more effective than similar treatments given only during reperfusion.