Sudden death during bating: cardiovascular collapse by experimental hyperthermia

建立了一种新的大鼠体温过高模型，模拟日本大鼠热水浴致猝死模型。在40摄氏度以上，老鼠被发现容易受到休克和死亡。血流动力学研究表明，过度高血压、心动过速和呼吸急促是最初的事件，然后发展为休克和心脏骤停。虽然这一序列已经在使用42-43摄氏度空气室的大鼠中暑模型中得到报道，但液体作为传热介质比空气更能更快地释放热能，这表明该模型可能是一种独特的模型，可用于考虑日本每年导致1.4万多人死亡的热水浸泡的风险。水温的死亡阈值为40摄氏度以上，体温的死亡阈值为42摄氏度。停止加热时，体温高于43摄氏度的大鼠出现休克并最终死亡，而体温低于42摄氏度的大鼠存活下来。细胞因子研究显示，在41℃水浴3小时后，除IL-6、TNF-α外，血浆中CINC_1水平升高，提示细胞因子级联反应参与了本实验模型的建立。

A new model for hyperthermia in rat model is produced and challenged simulating the hot bath immersion inducing sudden death in Japan. Above 40 degree C, rats are found to be vulnerable for shock and death. The homodynamic study showed that exaggerated hypertension, tachycardia and tachypnea are initial events which then progressed to shock and cardiac arrest. Although the sequence has already been reported in heat stroke model of rats using air-chamber of 42 to 43 degree C, liquid as heat transfer media is better to confer heat energy sooner than air, indicating this model may serve as an unique model useful for considering the risk of hot bath water immersion responsible more than 14,000 deaths annually in Japan. The threshold value for death of water temperature is more than 40 degree C, of body temperature is 42 degree C. On cessation of heating, rats with body temperature more than 43 degree C showed shock and eventually died, although those less than 42 degree C has survived. Cytokine study disclosed elevation of plasma CINC1, in addition to IL-6, TNF-alpha in plasma which was collected after bathing at 41 degree C for 3 hours, indicating activation of cytokine cascade is involved in this experimental model.