Kondratiev, Timofei V., Kristina Flemming, Eivind S. P. Myhre, Mikhail A. Sovershaev, and Torkjel Tveita. Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia? Am J Physiol Heart Circ Physiol 291: H441-H450, 2006. First published February 3, 2006 doi:10.1152/ajpheart.01229.2005.-It has been postulated that unsuccessful resuscitation of victims of accidental hypothermia is caused by insufficient tissue oxygenation. The aim of this study was to test whether inadequate O2 supply and/or malfunctioning O2 extraction occur during rewarming from deep/ profound hypothermia of different duration. Three groups of rats (n ϭ 7 each) were used: group 1 served as normothermic control for 5 h; groups 2 and 3 were core cooled to 15°C, kept at 15°C for 1 and 5 h, respectively, and then rewarmed. In both hypothermic groups, cardiac output (CO) decreased spontaneously by Ͼ50% in response to cooling. O2 consumption fell to less than one-third during cooling but recovered completely in both groups during rewarming. During hypothermia, circulating blood volume in both groups was reduced to approximately one-third of baseline, indicating that some vascular beds were critically perfused during hypothermia. CO recovered completely in animals rewarmed after 1 h (group 2) but recovered to only 60% in those rewarmed after 5 h (group 3), whereas blood volume increased to approximately three-fourths of baseline in both groups. Metabolic acidosis was observed only after 5 h of hypothermia (15°C). A significant increase in myocardial tissue heat shock protein 70 after rewarming in group 3, but not in group 2, indicates an association with the duration of hypothermia. Thus mechanisms facilitating O2 extraction function well during deep/profound hypothermia, and, despite low CO, O2 supply was not a limiting factor for survival in the present experiments. resuscitation; oxygen transport; oxygen consumption; heat shock protein 70; blood volume LITTLE IS KNOWN about the pathophysiology of tissue oxygenation during hypothermia in homeothermic experimental animals. Deranged tissue oxygenation has been postulated to be an important determinant for survival during prolonged (several hours) hypothermia as well as during rewarming after acute (a few hours) hypothermia. Hypothermia decreases the metabolic rate of a homeothermic organism. In clinical medicine, deliberate hypothermia has been used to depress metabolic rate and, thus, vulnerability of the tissue to ischemic damage. Cooling slows tissue body O 2 consumption (V O 2 ) and CO 2 production in parallel: ϳ4 -9% per 1°C (6,14,27). Short exposure time and low level of hypothermia are accepted as essential factors for a favorable outcome after rewarming. Thus, when hypothermia is used during, e.g., cardiac surgery, time and degree of temperature reduction are kept to a minimum. On the contrary, a victim of accidental hypothermia is frequently exposed to deep hypothermia for hours. This prolonged exposure and deep hypothermia are strongly related to failure of the...