三甲基氯化锡引发低血钾症的机制探讨  

The mechanism of hypokalemia induced by trimethyltin chloride

作　　者：唐小江[1] 黄建勋[2] 李来玉[2] 赖关朝[2] 邓莹玉[2] 越飞[2] 刘师琪[2] 

机构地区：[1]中山大学生命科学学院 [2]广东省职业病防治院毒理科,广州510300

出　　处：《中华劳动卫生职业病杂志》2001年第2期98-101,共4页Chinese Journal of Industrial Hygiene and Occupational Diseases

摘　　要：目的　探讨三甲基氯化锡 (trimethyltinchloride ,TMT)引发低血钾症的机制。方法　给SD大鼠腹腔注射TMT ,观察血浆钾、钠、氯及红细胞内钾的水平 ,红细胞膜Na+ K+ ATP酶、Ca2 + ATP酶及Mg2 + ATP酶活力 ,血浆醛固酮水平 ,动脉血pH值、CO2 分压 (pCO2 )等 6项血气分析指标 ,尿钾、钠、氯浓度及尿量 ,分析各指标与血钾变化的关系。结果　TMT为 46 .4mg/kg时 ,可在 0 .5h内导致血浆钾、钠浓度 [分别为 (4 .5 8± 0 .5 8)、(141.92± 2 .32 )mmol/L]迅速下降 ,与对照组 [分别为 (5 .86± 0 .6 1)、(147.5 6± 2 .90 )mmol/L]比较 ,差异有显著性 (P <0 .0 1) ;红细胞内钾浓度无变化 ;红细胞膜Na+ K+ ATP酶、Mg2 + ATP酶活力 [分别为 (0 .5 6 7± 0 .113)、(2 .6 35± 0 .331) μmolPi·(10 5RBC) -1·h-1]降低 ,与对照组 [分别为 (1.140± 0 .2 45 )、(1.0 0 0± 0 .34 3) μmolPi·(10 5RBC) -1·h-1]比较 ,差异有显著性 (分别为P <0 .0 1,P <0 .0 5 ) ;血浆醛固酮水平由 (5 0 .6 3± 6 4.2 8)pg/ml升高为 (5 13.5 1± 16 2 .75 )pg/ml,差异有显著性 (P <0 .0 1) ;动脉血pH值由 7.434降为 7.2 5 8;pCO2 由 2 9.6 2mmHg升至 45 .33mmHg ,差异有显著性 (P <0 .0 1) ;TMT(2 1.5mg/kg)可导致 2 4h尿量Objective To study the mechanism of hypokalemia induced by trimethyltin chloride(TMT). Methods SD rats were treated with TMT(ip).The main measurements included plasma K +,Na +,Cl - levels,intracellular potassium concentrantion of RBC,activities of Na + K + ATPase,Mg 2+ ATPase,Ca 2+ ATPase,plasma aldosterone levels,arterial blood pH,partial pressure of CO 2 (pCO 2),concentration of urinary potassium,sodium,chloride and urine volume in 24 hrs.All the indices were analysed to determine the possible relations to plasma K +. Results In rats treated with TMT(46.4 mg/kg),plasma K +,Na + levels[(4.58±0.58),(141.92±2.32)mmol/L respectively] were lower than those of control [(5.86±0.61),(147.56±2.90)mmol/L respectively] within 0.5 h( P <0.01);intracellular potassium concentration of RBC did not change( P >0.05);activities of Na + K + ATPase and Mg 2+ ATPase in RBC membrane were (0.567±0.113) and (2.635±0.331) μmol Pi·(10 5RBC) -1 ·h -1 respectively whereas those of control were (1.140±0.245) and (1.000±0.343) μmol Pi·(10 5RBC) -1 ·h -1 respectively( P <0.01, P <0.05);plasma aldosterone concentrations increased from (50.63±64.28)pg/ml to (513.51±162.75)pg/ml( P <0.01);arterial blood pH fell from 7.434 to 7.258 ( P < 0.01); pCO 2 raised from 29.62 mm Hg to 45.33 mm Hg( P <0.01).24 h urine volume,urinary potassium,sodium and chloride in rats treated with TMT(21.5 mg)were increased significantly[(23.68±9.38)ml,(1?120.88±416.19)μmol,(1?481.84±151.13)μmol and (1?227.57±366.65)μmol respectively] as compared to those of control[( 6.80 ±1.99)ml,(379.44±254.17)μmol,(978.67±279.98)μmol and (840.42±234.13)μmol respectively]( P < 0.01). Conclusion TMT could induce acute renal diuresis and rise of plasma aldosterone which may promote renal potassium excretion thus leading to hypokalemia and respiratory acidosis.Furthermore,the clinical manifestation of hypokalemia may be aggravated and death may occur due to respiratory fai

关 键 词：三四基氯化锡 低血钾症 作用机制 三四基氯化锡中毒 

分 类 号：R135.1[医药卫生—劳动卫生] R591.1[医药卫生—公共卫生与预防医学]