With the advent of sophisticated rewarming techniques, physiologic systems demonstrate great tolerance to hypothermia. Organs can be cooled, and in some cases frozen, leading to a decrease in metabolic demands and then rewarmed with little or no long-term damage. Not all cases of hypothermia are reversed with rewarming. The major challenge for extending the limits of tolerance to hypothermia is to ascertain the fundamental mechanisms that are unleashed upon rewarming. The microvasculature remains the key site for extending human tolerance to hypothermia. The currently favored hypothesis for frostbit- induced damage is that free radicals are released by reperfusion that subsequently alter vascular tone. Eventually, these changes cause failure of the microcirculation and endothelial cell damage, resulting in thrombosis and necrosis. It is probable that the same cascade of events that occurs in frostbite also occurs during rewarming of the hypothermic patient. Predicting which system will fail upon rewarming is difficult since in many cases the hypothermia is secondary to some underlying pathology. This review will focus on two aspects of tolerance to the cold: 1) the physiologic effects that occur during hypothermia, and 2) the role various forms of rewarming play in reversing hypothermia.