title: Studies on hypokalemia induced by trimethyltin chloride.
abstract: OBJECTIVE
  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.
  
  
  METHODS
  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+.
  
  
  RESULTS
  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).
  
  
  CONCLUSIONS
  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.
authors.affiliation: Department of Toxicology, Guangdong Provincial Center for Occupational Disease Prevention and Treatment, Guangzhou, 510300, China.
authors.forename: Xiao-Jiang
authors.initials: XJ
authors.lastname: Tang
authors.forename: Guan-Chao
authors.initials: GC
authors.lastname: Lai
authors.forename: Jian-Xun
authors.initials: JX
authors.lastname: Huang
authors.forename: Lai-Yu
authors.initials: LY
authors.lastname: Li
authors.forename: Ying-Yu
authors.initials: YY
authors.lastname: Deng
authors.forename: Fei
authors.initials: F
authors.lastname: Yue
authors.forename: Qing
authors.initials: Q
authors.lastname: Zhang
mesh_terms: D000818:Animals; D005260:Female; D007008:Hypokalemia / Q000139:chemically induced* / Q000662:veterinary; D007274:Injections, Intraperitoneal; D007674:Kidney Diseases / Q000139:chemically induced / Q000662:veterinary; D007928:Lethal Dose 50; D008297:Male; D051381:Rats; D017207:Rats, Sprague-Dawley; D012720:Severity of Illness Index; D014298:Trimethyltin Compounds / Q000494:pharmacology / Q000506:poisoning*
chemical_list: D014298:Trimethyltin Compounds; C040533:trimethyltin chloride