Maintaining intravenous volume mitigates hypothermia-induced myocardial dysfunction and accumulation of intracellular Ca2.

Previous research exploring pathophysiological mechanisms underlying circulatory collapse after rewarming victims of severe accidental hypothermia has documented post-hypothermic cardiac dysfunction and hypothermia-induced elevation of intracellular Ca2+ concentration ([Ca2+ ]i ) in myocardial cells. The aim of the present study was to examine if maintaining euvolaemia during rewarming mitigates cardiac dysfunction and/or normalizes elevated myocardial [Ca2+ ]i . A total of 21 male Wistar rats (300 g) were surface cooled to 15°C, then maintained at 15°C for 4 h, and subsequently rewarmed to 37°C. The rats were randomly assigned to one of three groups: (1) non-intervention control (n = 7), (2) dextran treated (i.v. 12 ml/kg dextran 70; n = 7), or (3) crystalloid treated (24 ml/kg 0.9% i.v. saline; n = 7). Infusions occurred during the first 30 min of rewarming. Arterial blood pressure, stroke volume (SV), cardiac output (CO), contractility (dP/dtmax ) and blood gas changes were measured. Post-hypothermic changes in [Ca2+ ]i were measured using the method of radiolabelled Ca2+ (45 Ca2+ ). Untreated controls displayed post-hypothermic cardiac dysfunction with significantly reduced CO, SV and dP/dtmax . In contrast, rats receiving crystalloid or dextran treatment showed a return to pre-hypothermic control levels of CO and SV after rewarming, with the dextran group displaying significantly better amelioration of post-hypothermic cardiac dysfunction than the crystalloid group. Compared to the post-hypothermic increase in myocardial [Ca2+ ]i in non-treated controls, [Ca2+ ]i values with crystalloid and dextran did not increase to the same extent after rewarming. Volume replacement with crystalloid or dextran during rewarming abolishes post-hypothermic cardiac dysfunction, and partially mitigates the hypothermia-induced elevation of [Ca2+ ]i .