Submitted on November 21, 2005
Accepted on January 30, 2006
Is oxygen supply a limiting factor for survival during rewarming from profound hypothermia?
Timofei V Kondratiev1*, Kristina Flemming1, Eivind S.P. Myhre2, Mikhail A Sovershaev3, and Torkjel Tveita4
1 Dept. of Anesthesiology, Institute of Clinical Medicine, University of Tromso, Tromso, Norway; Dept. of Medical Physiology, Institute of Medical Biology, University of Tromso, Tromso, Norway
2 Sect. of Cardiology, Dept. of Medicine, Soerlandet Hospital, Kristiansand, Norway
3 Dept. of Biochemistry, Institute of Medical Biology, University of Tromso, Tromso, Norway
4 Dept. of Anesthesiology, Institute of Clinical Medicine, University of Tromso, Tromso, Norway; Dept. of Medical Physiology, Institute of Medical Biology, University of Tromso, Tromso, Norway; Dept. of Anesthesiology, University Hospital of North Norway, Tromso, Norway
* To whom correspondence should be addressed. E-mail: timoteik{at}fagmed.uit.no.
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 oxygen supply and/or malfunctioning oxygen extraction occur during rewarming from deep/profound hypothermia of different duration. Three groups of rats (each n=7) were used. Group 1 served as normothermic control for 5 hrs, whereas group 2 and 3 were core cooled to 15°C, kept at this temperature for 1 or 5 hrs, respectively, and then rewarmed. In both hypothermic groups cardiac output (CO) decreased spontaneously in response to cooling by more than 50%. Oxygen consumption fell to less than 1/3 during cooling, but recovered completely in both groups during rewarming. During hypothermia circulating blood volume in both groups was reduced to approximately 1/3 of baseline value indicating that some vascular beds were critically perfused during hypothermia. If rewarmed after 1 hr, CO recovered completely (group 2), but if rewarmed after 5 hrs (group 3), CO recovered to only 60% whereas blood volume increased to approximately 3/4 of baseline in both groups. Metabolic acidosis was observed only following 5 hrs hypothermia (15°C). A significant increase in myocardial tissue heat shock protein 70 (HSP70) was measured after rewarming group 3, a result not seen in group 2 indicating that the increase is related to the duration of hypothermia. Thus, mechanisms facilitating oxygen extraction are well functioning during deep/profound hypothermia and despite low CO oxygen supply was not a limiting factor for survival in the present experiments.
