Pathophysiology of Non-Freezing Cold Injury

Cold injury is often associated with irreversible cell damage. To date, however, the pathophysiology of cold injury is not known. The present study examines the mechanism of such injury. New Zealand white rabbits were anesthetized with ketamine and xylazine and then ventilated using a Harvard ventilator. The femoral artery and vein were exposed. A flow probe was placed around the femoral artery which, in turn, was connected to a six channel recorder. A continuous display of EKG was obtained on lead II by connecting the limb leads to the same recorder. A thermocouple probe was inserted inside the leg to be cooled. After baseline measurements, one leg was cooled with a freezing mixture up to 0C, which was followed by rewarming. The other leg served as control. During the experiment, blood samples were withdrawn from the femoral artery and vein for the subsequent analysis of cretine kinaseCK, lactate dehydrogenaseLDH, and malonaldehyde MDA. At the end, salicylate was injected through the femoral vein to trap any hydroxyl radical OH formed. Our results indicated that local blood flow in cold exposed leg was reduced significantly, suggesting that cold injury was associated with ischemic insult. These results indicate that rewarming is associated with an episode of ischemiareperfusion with simultaneous generation of free radicals, which at least in part may be responsible for the cellular injury. Keywords Cold injury Ischemia Free radical.