三甲基氯化锡引起低血钾症的肾脏机制探讨  

Renal mechanism of hypokalemia induced by trimethyltin chloride

作　　者：唐小江[1] 宋静[2] 高彩凤[1] 杨晓君[1] 郭景惠[3] 陈仲宜[1] 周文良[3] 

机构地区：[1]广东省职业病防治院,广东广州510300 [2]山西医科大学,太原030001 [3]中山大学生命科学院,广州510275

出　　处：《中国职业医学》2006年第1期9-11,共3页China Occupational Medicine

基　　金：广东省医学科学技术研究基金项目(编号:B2002005)

摘　　要：目的探讨三甲基氯化锡(trim ethyltin ch loride,TMT)引起低血钾症的肾脏机制。方法将SD大鼠随机分成3组,每组10只,分别经腹腔注射TMT 0、10.0、21.5 m g/kg,测定0.5 h、1 d、3 d、6 d和11 d血浆的钾。将大鼠随机分成2组,每组10只,分别经腹腔注射TMT 0、10.0 m g/kg,测定1 d、6 d和11 d的24 h尿量和尿钾浓度。将大鼠随机分成6组,每组10只,分别经腹腔注射TMT 0、10.0 m g/kg,测定1 d、6 d和11 d的肾小管上皮细胞膜钠钾ATP酶的活力。结果大鼠腹腔注射TMT 10.0、21.5 m g/kg后0.5 h,血钾显著下降(P<0.05),6 d和11 d血钾仍低于正常水平(P<0.05);给予TMT 10.0 m g/kg后1 d、6 d和11 d,尿量先增后减、尿排总钾均显著增加(P<0.05);1 d、6 d和11 d肾小管上皮细胞膜钠钾ATP酶活力均显著低于对照组(P<0.01)。结论TMT引起低血钾症的主要原因是肾脏排钾持续增多,其机制与TMT引起肾小管细胞膜钠钾ATP酶活力下降,进而引起K+的重吸收下降有关。Objective To study the renal mechanism of hypokaJemia induced by trimethyltin chloride （TMT）. Methods SD rats were randomly divided into 3 groups （ 10 rats per group） and injected TMT 0, 10.0 and 21.5 mg/kg, respectively. Plasma potassium was analyzed at 0.5 h and at the 1st , 3rd, 6th and 1 l th day, Rats were randomly divided into 2 groups （10 rats per group） and injected TMT 0 and 10.0 mg/kg, respectively. Urine was collected for 24 h at the 1st, 6th and 11th day. The urine volume and the concentration of urine potassium were measured. Rats were randomly divided into 6 groups （ 10 rats per group） and injected TMT 0 and 10.0 mg/kg, respectively. Renal epidermis membrane was separated at the 1st, 6th and 11th day and the Na^＋-K^＋ -ATPase activities of it were analyzed. Results Both in the 10.0 mg/kg and 21.5 mg/kg groups, plasma K^＋ level dropped quickly half an hour after TMT treatment （P 〈 0.05）and didnt recover until the experiment ended at the 11 th day. 24h total urinary potassium of 1,6 and 11 days after the rats were treated with TMT（10.0mg/kg） increased significantly in comparison with those in the controls （P 〈 0.05）. The Na^＋ -K^＋ ATPase activities in renal epidermis membrane depressed remarkably（P 〈0.01） in 1, 6 and 11 days after TMT treatment（ 10.0 mg/kg）. Conclusion The available evidence suggested that promoting potassium leakage from kidney continuously would be the main pathogeny of hypokalemia induced by TMT. It would be one of the mechanism that TMT could depress the activities of Na^＋-K^＋ -ATPase in renal epidermis membrane, consequently reduce the reabsorption of K ＋.

关 键 词：三甲基氯化锡 低血钾症 肾脏 钠钾ATP酶 

分 类 号：R135.1[医药卫生—劳动卫生]