Tang Xiao-Jiang, Lai Guan-Chao, Huang Jian-Xun, Li Lai-Yu, Deng Ying-Yu, Yue Fei, Zhang Qing
Department of Toxicology, Guangdong Provincial Center for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
Biomed Environ Sci. 2002 Mar;15(1):16-24.
To determine the possible relationship between plasma potassium concentration and severity of acute trimethyltin chloride (TMT) poisoning and to assess the mechanism of TMT induced hypokalemia.
SD rats were treated with various dosages of TMT (i.p.). All the indices were measured and analysed for determining their possible relations with plasma K+.
With increase of dosage, the plasma K+ level dropped rapidly, and deaths appeared more quickly. The LD50 of TMT (i.p.) was 14.7 mg/kgbw. In the low dosage group (10 mg/kgbw), the plasma K+ level dropped slowly with the lowest dosage on day 6 (4.85 mmol/L). It rose again on day 11 (5.06 mmol/L), and recovered on day 28. The poisoning signs corresponded with decline of the span of K+ level. The plasma Na+ level dropped half an hour after TMT treatment, but recovered 24 h later. In the high dosage group (46.4 mg/kgbw), the levels of plasma K+ and Na+ fell rapidly within half an hour (P < 0.05), the intracellular potassium concentration of RBC did not decrease obviously (P > 0.05), the activities of Na(+)-K(+)-ATPase and Mg(2+)-ATPase in RBC membrane were depressed remarkably (P < 0.01, P < 0.05, respectively), the plasma aldosterone concentrations rose as high as tenfold (P < 0.01), the arterial blood pH fell from 7.434 to 7.258 (P < 0.01), pCO2 was raised from 29.62 to 45.33 mmHg (P < 0.01). In the 24 h urine test, when rats were treated with TMT (21.5 mg/kgbw, i.p.), urine volume, urinary potassium, sodium and chloride increased significantly in comparison with those in the controls (P < 0.01).
TMT could induce hypokalemia in SD rats. The available evidence suggests that TMT can induce acute renal leakage of potassium. At the same time, a significant rise of plasma aldosterone may play an important role in promoting potassium leakage from kidney to result in severe hypokalemia with inhaling acid-base abnormalities produced, which aggravate the poisoning symptoms. In the end the rats would die of respiratory failure.
确定血浆钾浓度与急性三甲基氯化锡（TMT）中毒严重程度之间的可能关系，并评估TMT诱导低钾血症的机制。
用不同剂量的TMT（腹腔注射）处理SD大鼠。测量并分析所有指标，以确定它们与血浆K⁺的可能关系。
随着剂量增加，血浆K⁺水平迅速下降，死亡出现得更快。TMT（腹腔注射）的半数致死量（LD50）为14.7mg/kg体重。在低剂量组（10mg/kg体重）中，血浆K⁺水平下降缓慢，在第6天降至最低剂量（4.85mmol/L）。在第11天再次上升（5.06mmol/L），并在第28天恢复。中毒体征与K⁺水平跨度的下降相对应。TMT处理后半小时血浆Na⁺水平下降，但24小时后恢复。在高剂量组（46.4mg/kg体重）中，血浆K⁺和Na⁺水平在半小时内迅速下降（P<0.05），红细胞内钾浓度没有明显降低（P>0.05），红细胞膜上Na⁺-K⁺-ATP酶和Mg²⁺-ATP酶的活性显著降低（分别为P<0.01，P<0.05），血浆醛固酮浓度升高至原来的十倍（P<0.01），动脉血pH从7.434降至7.258（P<0.01），pCO₂从29.62mmHg升高至45.33mmHg（P<0.01）。在24小时尿液检测中，当用TMT（21.5mg/kg体重，腹腔注射）处理大鼠时，与对照组相比，尿量、尿钾、尿钠和尿氯显著增加（P<0.01）。
TMT可诱导SD大鼠低钾血症。现有证据表明，TMT可导致急性肾钾泄漏。同时血浆醛固酮显著升高可能在促进钾从肾脏泄漏中起重要作用，导致严重低钾血症并伴有酸碱平衡异常，加重中毒症状。最终大鼠死于呼吸衰竭。
