CAJ | 학술논문

目的　探讨三甲基氯化锡(trimethyltin chloride,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46.4 mg/kg时，可在0.5 h内导致血浆钾、钠浓度［分别为(4.58±0.58)、(141.92±2.32)mmol/L］迅速下降，与对照组［分别为(5.86±0.61)、(147.56±2.90)mmol/L］比较，差异有显著性(P<0.01)；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(0.567±0.113)、(2.635±0.331)μmol Pi*(105RBC)-1*h-1］降低，与对照组［分别为(1.140±0.245)、(1.000±0.343)μmol Pi*(105RBC)-1*h-1］比较，差异有显著性(分别为P<0.01,P<0.05)；血浆醛固酮水平由(50.63±64.28)pg/ml升高为(513.51±162.75)pg/ml，差异有显著性(P<0.01)；动脉血pH值由7.434降为7.258；pCO2由29.62 mm Hg升至45.33 mm Hg，差异有显著性(P<0.01)；TMT(21.5 mg/kg)可导致24 h尿量(23.68±9.38)ml和尿钾、钠、氯排出量［(1*!120.88±416.19)、(1*!481.84±151.13)、(1*!227.57±366.65)μmol］增加，与对照组［(6.80±1.99)ml和(379.44±254.17)、(978.67±279.98)、(840.42±234.13)μmol］比较，差异有显著性(P<0.01)。结论　TMT具有急性利尿作用，并可迅速升高血浆醛固酮水平，促进钾经肾排出，从而引起血钾下降，并进一步引起呼吸性酸中毒，加重低血钾的临床表现，最终可导致呼吸衰竭而死亡。
목적　탐토삼갑기록화석(trimethyltin chloride,TMT)인발저혈갑증적궤제。방법　급SD대서복강주사TMT,관찰혈장갑、납、록급홍세포내갑적수평，홍세포막Na+-K+-ATP매、Ca2+-ATP매급Mg2+-ATP매활력，혈장철고동수평，동맥혈pH치、CO2분압(pCO2)등6항혈기분석지표，뇨갑、납、록농도급뇨량，분석각지표여혈갑변화적관계。결과　TMT위46.4 mg/kg시，가재0.5 h내도치혈장갑、납농도［분별위(4.58±0.58)、(141.92±2.32)mmol/L］신속하강，여대조조［분별위(5.86±0.61)、(147.56±2.90)mmol/L］비교，차이유현저성(P<0.01)；홍세포내갑농도무변화；홍세포막Na+-K+-ATP매、Mg2+-ATP매활력［분별위(0.567±0.113)、(2.635±0.331)μmol Pi*(105RBC)-1*h-1］강저，여대조조［분별위(1.140±0.245)、(1.000±0.343)μmol Pi*(105RBC)-1*h-1］비교，차이유현저성(분별위P<0.01,P<0.05)；혈장철고동수평유(50.63±64.28)pg/ml승고위(513.51±162.75)pg/ml，차이유현저성(P<0.01)；동맥혈pH치유7.434강위7.258；pCO2유29.62 mm Hg승지45.33 mm Hg，차이유현저성(P<0.01)；TMT(21.5 mg/kg)가도치24 h뇨량(23.68±9.38)ml화뇨갑、납、록배출량［(1*!120.88±416.19)、(1*!481.84±151.13)、(1*!227.57±366.65)μmol］증가，여대조조［(6.80±1.99)ml화(379.44±254.17)、(978.67±279.98)、(840.42±234.13)μmol］비교，차이유현저성(P<0.01)。결론　TMT구유급성이뇨작용，병가신속승고혈장철고동수평，촉진갑경신배출，종이인기혈갑하강，병진일보인기호흡성산중독，가중저혈갑적림상표현，최종가도치호흡쇠갈이사망。
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,Mg2+-ATPase,Ca2+-ATPase,plasma aldosterone levels,arterial blood pH,partial pressure of CO2 (pCO2),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 Mg2+-ATPase in RBC membrane were (0.567±0.113) and (2.635±0.331)μmol Pi*(105RBC)-1*h-1 respectively whereas those of control were (1.140±0.245) and (1.000±0.343) μmol Pi*(105RBC)-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);pCO2 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 failure.