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  • Title: Myocardial mechanical dysfunction and calcium overload following rewarming from experimental hypothermia in vivo.
    Author: Kondratiev TV, Wold RM, Aasum E, Tveita T.
    Journal: Cryobiology; 2008 Feb; 56(1):15-21. PubMed ID: 17983615.
    Abstract:
    Rewarming patients from accidental hypothermia are regularly complicated with cardiovascular instability ranging from minor depression of cardiac output to fatal circulatory collapse also termed "rewarming shock". Since altered Ca2+ handling may play a role in hypothermia-induced heart failure, we studied changes in Ca2+ homeostasis in in situ hearts following hypothermia and rewarming. A rat model designed for studies of the intact heart in a non-arrested state during hypothermia and rewarming was used. Rats were core cooled to 15 degrees C, maintained at 15 degrees C for 4h and thereafter rewarmed. As time-matched controls, one group of animals was kept at 37 degrees C for 5h. Total intracellular myocardial Ca2+ content ([Ca2+]i) was measured using 45Ca2+. Following rewarming we found a significant reduction of stroke volume and cardiac output compared to prehypothermic control values as well as to time-matched controls. Likewise, we found that hypothermia and rewarming resulted in a more than six-fold increase in [Ca2+]i to 3.01+/-0.43 micromol/g dry weight compared to 0.44+/-0.05 micromol/g dry weight in normothemia control. These findings indicate that hypothermia-induced alterations in the Ca2+-handling result in Ca2+ overload during hypothermia, which may contribute to myocardial failure during and after rewarming.
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