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Mechanisms underlying cardiac contractile dysfunction during and after rewarming from hypothermia remain largely unknown. We have previously reported myocardial post-hypothermic calcium overload to be the culprit. The aim of the present study was to measure changes in myocardial [Ca2+]i during graded hypothermia and after rewarming in an anesthetized, intact rat model, using the 45Ca2+ technique.Rats were randomized and cooled to 15 °C. Hearts were excised and perfusion-washed to remove extracellular calcium after 0.5 h of hypothermia (n = 9), 4 h of hypothermia (n = 8), and after 4 h of hypothermia and 2 h rewarming (n = 9). A normothermic group, kept at 37 °C for 5 h, served as control (n = 6). [Ca2+]i was determined in perchloric acid extracts of heart tissue. Spontaneous cardiac electromechanic work was maintained during hypothermia without cardiac arrest or ischaemia.Between 0.5 and 4 h at 15 °C, a six-fold increase in cardiac [Ca2+]i was observed (0.55 ± 0.10 vs. 2.93 ± 0.76 μmol (g dry wt)−1). Rewarming resulted in a 33% decline in [Ca2+]i, but the actual value was significantly above the value measured in control hearts.We show that calcium overload is a characteristic feature of the beating heart during deep hypothermia, which aggravates by increasing duration of exposure. The relatively low decline in [Ca2+]i during the rewarming period indicates difficulties in recovering calcium homoeostasis, which in turn may explain cardiac contractile dysfunction observed after rewarming.