Objectives To determine the possible relationship between plasma potassiumconcentration and severity of acute trimethyltin chloride (TMT) poisoning and to assess themechanism of TMT induced hypokalemia. Methods SD rats were treated with variousdosages of TMT (ip). All the indices were measured and analysed for determing theirpossible relations with plasma K+. Results With increase of dosage, the plasma K+ leveldropped rapidly, and deaths appeared more quickly. The LD50 of TMT (ip) was 14.7 mg/kgbw. In the low dosage group (10 mg/kgbw), the plasma K+ level dropped slowly with thelowest dosage on day 6 (4.85 mmol/L). It rose again on day 11 (5.06 mmol/L), and recoverdon day 28. The poisoning signs corresponded with decline of the span of K+ level. The plasmaNa+ level dropped half an hour after TMT treatment, but recovered 24 h later. In the highdosage group (46.4 mg/kgbw), the levels of plasma K+ and Na+ fell rapidly within half anhour (P0.05), the activities of Na+-K+-ATPase and Mg2+-ATPase in RBC membrane weredepressed remarkably (P<0.01, P<0.05, respectively), the plasma aldosterone concentrationsrose 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 weretreated with TMT (21.5 mg/kgbw, ip), urine volume, urinary potassium, sodium and chlorideincreased significantly in comparison with those in the controls (P<0.01). Conclusion TMTcould induce hypokalemia in SD rats. The available evidence suggests that TMT can induceacute renal leakage of potassium. At the same time, a significant rise of plasma aldosteronemay play an important role in promoting potassium leakage from kidney to result in severehypokalemia with inhaling acid-base abnormalities produced, which aggravate the poisoningsymptoms. In the end the rats would die of respiratory failure.
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