McIvor M E, Cummings C E, Mower M M, Wenk R E, Lustgarten J A, Baltazar R F, Salomon J
Ann Emerg Med. 1987 Jul;16(7):777-81. doi: 10.1016/s0196-0644(87)80573-5.
The mechanism of sudden cardiac death following acute fluoride intoxication has been thought to result from profound hypocalcemia produced by the precipitation of calcium fluoride salts. In studies of a canine model, the onset of lethal ventricular arrhythmias was temporally more associated with an elevation of serum potassium than with a drop in serum calcium. Fluoride-induced hyperkalemia could not be prevented with glucose, insulin, or bicarbonate. In the erythrocytes, a five-minute exposure to 10 mM NaF caused a 50% increase in extracellular potassium concentrations after 12 hours compared to control erythrocyte suspensions (P less than .001). The total potassium efflux after 12 hours of incubation was linearly related to the log of fluoride contact time (r, 0.886; P less than .001). The treatment of fluoride-induced hyperkalemia may depend on removal of fluoride and potassium.
急性氟中毒后心源性猝死的机制被认为是由氟化钙盐沉淀导致的严重低钙血症所致。在犬类模型研究中，致命性室性心律失常的发作在时间上与血清钾升高的关联比与血清钙降低的关联更大。氟诱导的高钾血症无法通过葡萄糖、胰岛素或碳酸氢盐预防。在红细胞中，与对照红细胞悬液相比，10 mM氟化钠处理5分钟后，12小时时细胞外钾浓度增加了50%（P小于0.001）。孵育12小时后的总钾外流与氟接触时间的对数呈线性相关（r，0.886；P小于0.001）。氟诱导的高钾血症的治疗可能取决于氟和钾的清除。
