Rewarming from accidental hypothermia is often complicated by "rewarming shock", characterized by low cardiac output (CO) and a sudden fall in peripheral arterial pressure. In this study we tested if epinephrine (Epi) is able to prevent rewarming shock when given intravenously during rewarming from experimental hypothermia in doses tested to elevate CO and induce vasodilation, or lack of vasodilation, during normothermia. A rat model designed for circulatory studies during experimental hypothermia and rewarming was used. A total of six groups of animals were used: normothermic groups 1, 2 and 3 for dose-finding studies and hypothermic groups 4, 5 and 6. At 20 and 24°C during rewarming group 4 (low dose Epi) and group 5 (high dose Epi) received bolus injection of 0.1 µg and 1.0 µg Epi respectively. At 28°C Epi infusion was started in group 4 and 5 with 0.125 µg/min and 1.25 µg/min respectively. Group 6 served as saline control. After rewarming both CO and SV were restored in group 4, in contrast to group 5 and group 6 where both CO and SV remained significantly reduced (30%). TPR was significantly higher in group 5 during rewarming from 24 to 34°C, compared to group 4 and 6. This study shows that, in contrast to normothermic conditions, Epi infused during hypothermia induces vasoconstriction rather than vasodilation combined with lack of CO elevation. The apparent dissociation between myocardial and vascular responses to Epi at low temperatures may be related to hypothermia-induced myocardial failure and changes in temperature dependent adrenoreceptor affinity.