定标时间对血清钾钠氯测定结果影响

目的：选择VITR∮S250型化学分析仪的最佳定标时间，为临床提供准确数据。方法：在换参比液后第一天、第二天、第三天时分别对VITR∮S250进行K^ 、Na^ 、Cl^-离子定标，每次定标后对PV1进行K^ 、Na^ 、Cl^-检测。结果：换参比液后第一天测定Na^ 结果大部分在PV1均值以下分布且严重失控，第三天测定Na^ 结果大部分在PVl均值上分布且四次失控，第二天测定Na^ 结果在PV1均值上下分布，仅一次失控。结论：换参比液后第二天是最佳定标时间，能确保检验结果的准确性。     

不同检测系统血清钾钠氯结果比对与临床可接受性分析

目的 分析比对不同生化检测系统测定血清钾、钠、氯结果,探讨其结果的可比性.方法 参照美国临床实验室标准化委员会(NCCLS)EP9-A2文件要求,以强生VITROS 250 干式生化分析仪检测系统为比较方法,OlympusAU640生化分析仪检测系统为实验方法,应用两个不同检测系统检测不同浓度的患者血清钾、钠、氯,判断不同检测系统的临床可接受性.结果 两个检测系统检测钾、钠、氯结果比较,差异无统计学意义(P>0.05),临床可接受性能评价均在可接受范围内,即检验结果具有可比性.结论 同一实验室不同检测系统进行同一项目检测时,应进行方法比对和偏倚评估,以保证检验结果的可比性.     

急性缺血性脑血管病患者应激性高血糖、血清钾、钠、氯的变化及其与病情轻重、预后关系

目的：探讨急性缺血性脑血管病患者应激性高血糖、血清钾、钠、氯的变化及其与病情轻重、预后关系。方法：本文对我院神经内科2004年5月～2006年5月住院急性缺血性脑血管病患者248例进行研究，于入院次日晨检测空腹血糖、血清钾、钠、氯，观察血糖、血钠、血氯、血钾值的变化及其与病情轻重、预后关系。结果：（1）急性缺血性脑血管病患者易出现应激性高血糖、低钠血症、低氯血症、低钾血症；（2）高血糖组死亡率明显高于非高血糖组；死亡组的血糖均值亦显著高于存活组；统计学上差异有显著性。（3）低血钠、低血氯组中的中、重度患者显著多于正常血钠、血氯组；与正常血钠、血氯组相比，高血钠、高血氯组患者在病情轻重及预后方面差异均无显著性，但血钠、血氯显著升高时，死亡率明显增加。与正常血钾组相比。低血钾组中患者在病情轻重及预后方面差异无显著性，但血钾明显降低时，病死率增加。高血钾组患者在病情轻重和正常血钾组相比差异无显著性，但病死率则明显高于正常血钾组。结论：急性缺血性脑血管病患者存在应激反应，急性缺血性脑血管病患者应激性高血糖、低钠血症、低氯血症可以作为判断急性缺血性脑血管病病情较轻重、预后评估的指标之一。高钠血症、高氯血症、高钾血症、低钾血症与病情轻重及预后方面差异无显著性，但当出现严重的高钠血症、高氯血症、高钾血症、低钾血症时，病死率明显增加。     

应用多层膜电极法测定血清钾钠氯

近年来,干化学分析及其检测仪器的研制,开发和应用得到迅速发展。美国柯达公司生产的Kodak Ektachem DT－60干式生化分析仪及配套用多层膜胶片,受到广大检验工作者的认可和好评[1]。该仪器与DT－60主机配套的DTE组件,采用多层膜电极法测定血清中钾钠氯浓度。经我们一年来的应用,取得比较满意的效果,各种实验数据已达到了直接离子选择电极法的分析水平,在急诊检验工作中发挥了重要作用。特作如下报道： 1 材料与方法 1．1 仪器材料 1．1．1 Kodak Ektachem DT－60干式生化分析仪美国柯达公司产品 1．1．2 DTE组件：与DT－…     

三种不同检测系统钾钠氯测定结果的比对研究

目的通过方法学比较和偏倚评估,探讨不同检测系统钾钠氯检测结果的可比性。方法根据EP9-A2文件,以重复性和准确性最佳的Vitros350系统（用A表示）为目标系统,日立7600检测系统（用B表示）、上海富升Easyplus电解质检测系统（用C表示）为实验系统,检测40份患者新鲜血清的钾钠氯,以美国临床实验室修正法规（CLIA’88）规定的室间质量评价允许范围的1/2为临床可接受范围,判断不同检测系统的可比性。结果各检测系统测定钾钠氯的批内、批间变异系数均小于2%;各检测系统间的相关系数均大于0.975,B、C两系统与A系统比较：B系统的钾钠氯及C系统氯符合要求,C系统的钾部分超过及钠全部超过CLIA’88规定的1/2。结论三个检测系统测定钾钠氯的精密度符合临床要求,临床接受性能评价B系统尚可,但C系统有部分项目或全部项目不可比性。实验室应经常进行同一项目不同检测系统间的偏倚评估,判断临床接受性能,采取整改措施,保证结果的可比性。     

内源性干扰物质对酶法测定钾钠氯结果的影响

目的评价黄疸、溶血、脂血、尿毒症等异常标本中内源性干扰物质对酶法测定血清中钾钠氯结果的影响。方法依据美国国家临床实验室标准化委员会(NCCLS)的EP 7-P文件,分别用间接离子选择性电极(ISE)和酶法测定正常对照组(非黄疸、溶血、脂血)、黄疸组、溶血组、脂血组、尿毒症组标本中钾钠氯,对结果进行统计学分析。结果正常对照组,酶法钠氯均高于ISE(P<0.05),钾在两种方法间无差异;溶血、黄疸对酶法测定钾钠氯均无干扰(P>0.05);脂血(TG<15mm o l/L)对酶法测定钾氯无干扰,钠呈负偏差,但酶法不能测定严重脂血标本(TG>15 mm o l/L)中钾钠氯,脂血标本中钠偏倚与甘油三酯、胆固醇浓度不相关(r=0.06,r=0.10);尿毒症组样品中钾与对照组呈负偏差(P<0.05),与CREA、BUN的浓度间弱相关(r=0.31,r=0.26),而尿毒症组标本中钠氯较正常对照组呈正偏差(P<0.05),与CREA、BUN浓度间无相关性(r=0.07,r=0.05)。结论溶血、黄疸、轻中度脂血对酶法测定钾钠氯无干扰,但不能用于分析严重脂血标本、尿毒症标本的钾钠氯测定。     

三种不同检测系统钾钠氯测定结果的比对研究

目的通过方法学比较和偏倚评估,探讨不同检测系统钾钠氯检测结果的可比性。方法根据EP9-A2文件,以重复性和准确性最佳的Vitros350系统（用A表示）为目标系统,日立7600检测系统（用B表示）、上海富升Easyplus电解质检测系统（用C表示）为实验系统,检测40份患者新鲜血清的钾钠氯,以美国临床实验室修正法规（CLIA’88）规定的室间质量评价允许范围的1/2为临床可接受范围,判断不同检测系统的可比性。结果各检测系统测定钾钠氯的批内、批间变异系数均小于2%;各检测系统间的相关系数均大于0.975,B、C两系统与A系统比较：B系统的钾钠氯及C系统氯符合要求,C系统的钾部分超过及钠全部超过CLIA’88规定的1/2。结论三个检测系统测定钾钠氯的精密度符合临床要求,临床接受性能评价B系统尚可,但C系统有部分项目或全部项目不可比性。实验室应经常进行同一项目不同检测系统间的偏倚评估,判断临床接受性能,采取整改措施,保证结果的可比性。     

应用酶法和电极法测定血清钾钠氯的实验对比

为了解酶法分析Ｋ＾＋、Ｎａ＾＋、Ｃｌ＾－的特点，应用电极法进行了实验对比，结果二种方法线怀范围和平均回收率均符合要求，精密度实验批内和批间ＣＶ值均在允许范围，但电极法明显优于酶法，同二种方法测定Ｋ＾＋、Ｎａ＾＋、Ｃｌ＾－的相关系数分别为０．９７６７，０．９７８５和０．９５２５，且差异不显著（Ｐ〉０．０５），溶血样品对二种方法测Ｋ＾＋均有明显正干扰，高脂血样品对电极法无干扰，而对酶法测Ｎａ＾＋，ＣＩ     

惰性分离胶管保存标本对钾、钠、氯检测结果的影响

目的:研究惰性分离胶管采集和保存钾(K+)、钠(Na+)、氯(Cl-)标本的可行性.方法:随机选择患者标本40例,采用惰性分离胶管和干燥管(无抗凝)采集同一患者血液标本,待血液凝固后立即离心,各取出150μL血清到Eppendorf管(简称Ep管)冷冻保存;再分别于2,4,6,8,24h后从惰性分离胶管中取出150μL血清到Ep管中冷冻保存,检测并比较上述血清的K+、Na+、Cl-浓度.结果:惰性分离胶管和干燥管离心后0hK+、Na+、Cl-结果差异无统计学意义(P>0.05),惰性分离胶管的2,4,6,8,24hK+、Na+、Cl-检测结果与0hK+、Na+、Cl-检测结果差异也无统计学意义(P>0.05).结论:使用惰性分离胶管不会影响K+、Na+、Cl-的检测结果,且可以防止K+、Na+、Cl-浓度的改变,能有效保存这些标本.     

血清中钾、钠、氯、钙、碳酸氢盐的同时测量

研制了一种同时测量人血清中钾、钠、氯、钙、碳酸氢盐的自动分析系统，该系统用离子选择电极法测量血清样品中的钾、钠、氯、钙，用动态量压法测量血清中的碳酸氢盐。样品用量150μl，分析时间小于90s，系统具有测量参数多，分析速度快，样品用量少，测量准确，操作方便等特点，完全满足临床检验的要求。     

Na+, K+, H+, Cl-, and Ca2+ concentrations in cystic fibrosis eccrine sweat in vivo and in vitro

Sweat Na+, K+, H+, Cl-, Ca2+, and protein concentrations were reexamined with the use of three methods; namely, in vitro sweat induction from isolated single sweat glands, intradermal methacholine-induced sweating, and thermally induced sweating. [Na+] and [K+] in the primary sweat induced in vitro were nearly isotonic to the bath in both cystic fibrosis (CF) and control. In CF the [Na+] in both proximal ductal and skin surface sweat was always higher than 100 mmol/L. However, [Na+] never reached the isotonic level of 151 mmol/L, even at the highest sweat rate. Thus Na+ absorption never saturates, suggesting that the net NaCl absorption may increase with increasing sweat rate. pH of the primary sweat was 7.13 for CF and 7.29 for control, which corresponds to a [HCO3-] of 7.3 and 10.5 mmol/L, respectively. [Cl-] in the primary sweat was hypertonic (134 mmol/L for CF and 129 mmol/L for control) to the bath (118.4 mmol/L). In CF, ductal acidification of sweat occurred normally during intradermal methacholine-induced sweating, whereas ductal acidification of sweat was much higher in control than in CF in thermally induced sweating. [K+] in CF was higher in the skin surface sweat but not in the proximal duct sweat, suggesting that the predominant site of K+ secretion in CF may be in the distal duct. [K+] in the intradermal methacholine-induced sweat was much higher than that of thermally induced sweat in both CF and control samples. Free but not total [Ca2+] was also increased in CF skin surface sweat. The sweat protein concentration was the same in both CF and control samples. The mechanisms of the different electrolyte concentrations in CF sweat remain to be studied. However, the present observations will provide the basis for future studies on normal and abnormal regulation of membrane transport in CF sweat glands.     

Effect of cooling on the intracellular concentrations of Na+, K+ and Cl- in cultured human endothelial cells

Cooling is accepted as a practical way of lowering cell metabolism in vein grafts during coronary by-pass surgery. We have previously shown that low temperature causes endothelial cells to become detached, both in in vitro and in vein graft. In this study we have looked at the effect of cold on the concentrations of intra- and extracellular electrolytes. Human endothelial cells were grown on titanium grids for electron microscopy. The cells were incubated for 30 min at 37 degrees, 20 degrees, and 4 degrees C with cell culture medium containing human serum, and at 20 degrees and 4 degrees C with heparinized sodium acetate solution with serum, frequently used for flushing and distending vein grafts. Freeze-dried cells were then subjected to elemental X-ray microanalysis. The ambient fluid was analysed by flame photometry. At 20 degrees and 4 degrees C, intracellular concentration of sodium increased, and potassium decreased, compared with controls (37 degrees C). The changes in sodium concentrations were aggravated when cell culture medium was replaced by heparinized sodium acetate. The intracellular chloride concentration did not change when cells were stored in cold cell culture medium. The extracellular concentration of potassium increased with increasing incubation time at 4 degrees C. The connection between these findings and cell detachment is discussed.     

Race and sex differences in erythrocyte Na+, K+, and Na+-K+-adenosine triphosphatase.

Several reports indicate that erythrocytes (RBCs) from blacks and men have higher sodium concentrations than those from whites and women. One possible mechanism to explain this finding is a difference in the activity of Na+-K+-ATPase. To explore this possibility, we have studied the Na+ and K+ kinetics of RBC Na+-K+-ATPase and RBC Na+ and K+ concentrations in 37 normotensive blacks and whites, both males and females. The maximal initial reaction velocity (Vmax) values for RBC Na+-K+-ATPase were lower in blacks and men as compared with whites and women. Higher RBC Na+ levels were observed in blacks and males vs. whites and females. Significant inverse correlations were noted between the Na+-K+-ATPase activity and RBC Na+ concentrations. These findings indicate that cellular Na+ homeostasis is different in blacks and men as compared with whites and women. Since higher RBC Na+ concentrations have also been observed in patients with essential hypertension as compared with normotensive subjects, the higher intracellular Na+ concentrations in blacks and men may contribute to the greater predisposition of these groups to essential hypertension.     

Cytochemical localization of Na+, K+-ATPase in the rat hepatocyte.

The enzyme Na+,5+-ATPase was cytochemically localized in the rat hepatocyte by a modification of the Ernst potassium-dependent nitrophenyl phosphatase technique. Measurement of nitrophenol release from 50-micrometer liver slices confirmed the presence of ouabain-inhibitable nitrophenyl phosphatase activity that increased over the 30-min incubation period. Electron micrographs demonstrated that sinusoidal and lateral membrane reaction product deposition was K+-dependent, Mg++-dependent, inhibited by ouabain but not by alkaline phosphatase inhibitors, and was localized to the cytoplasmic side of the membrane. In contrast, canalicular reaction product was K+-independent, Mg++-dependent, inhibited by alkaline phosphatase inhibitors but not by ouabain, and was localized to the luminal side of the membrane. These findings indicate that Na+,K+-ATPase is localized to the sinusoidal and lateral portions of the rat hepatocyte plasma membrane and is not detectable on the bile canaliculus where alkaline phosphatase is confined. This basolateral localization of Na+,K+-ATPase is similar to that found in epithelia where secretion is also directed across the apical membrane.     

Optimal conditions for measurement of Na+,K+-ATPase activity of human leucocytes

The Na+,K+-ATPase activity of human leucocytes was assayed by measuring the release of inorganic phosphate (Pi) from ATP. The maximum enzyme activity was achieved under the following conditions: concentration (mmol/l), Tris/HCl 50, Na 100, K 15, ATP 5, Mg 7, EDTA 1; pH 7.2 and temperature 37 degrees C, were optimal. Ouabain showed maximal inhibition at a concentration of 10-100 mumol/l. Ethanol, the solvent for ouabain, had a dose-related inhibitory effect. Heparin or citrate used as an anticoagulant gave similar results. Leucocyte samples could be stored at -20 degrees C for up to 6 days without loss of activity. Hypotonic lysis had advantages over sonication as the technique for cell disruption. The leucocyte Na+,K+-ATPase enzyme activity in healthy subjects was 186 mumol of Pi h-1g-1 of protein (median) with a range 136-243 mumol of Pi h-1g-1 of protein. The within-batch coefficient of variation was 6.4% and the between-batch precision was 9.6%.     

Vasoactive intestinal polypeptide-induced chloride secretion by a colonic epithelial cell line. Direct participation of a basolaterally localized Na+,K+,Cl- cotransport system.

We have used a well-differentiated human colonic cell line, the T84 cell line, as a model system to study the pathways of cellular ion transport involved in vasoactive intestinal polypeptide (VIP)-induced chloride secretion. A modified Ussing chamber was used to study transepithelial Na+ and Cl- fluxes across confluent monolayer cultures of the T84 cells grown on permeable supports. In a manner analogous to isolated intestine, the addition of VIP caused an increase of net Cl- secretion which accounted for the increase in short circuit current (Isc). The effect of VIP on Isc was dose dependent with a threshold stimulation at 10(-10) M VIP, and a maximal effect at 10(-8) M. Bumetanide prevented or reversed the response to VIP. Inhibition by bumetanide occurred promptly when it was added to the serosal, but not to the mucosal bathing media. Ion replacement studies demonstrated that the response to VIP required the simultaneous presence of Na+, K+, and Cl- in the serosal media. Utilizing cellular ion uptake techniques, we describe an interdependence of bumetanide-sensitive 22Na+, 86Rb+, and 36Cl- uptake, which is indicative of a Na+,K+,Cl- cotransport system in this cell line. This transport pathway was localized to the basolateral membrane. Extrapolated initial velocities of uptake for each of the three ions was consistent with the electroneutral cotransport of 1 Na+:1 K+ (Rb+):2 Cl-. Our findings indicate that VIP-induced Cl- secretion intimately involves a bumetanide-sensitive Na+,K+,Cl- cotransport system which is functionally localized to the basolateral membrane.     

Investigations on the Na+, K+-pump in erythrocytes of patients with renal hypertension

The ouabain-sensitive 42K+ flux from an artificial medium into erythrocytes was measured in 29 control subjects, 66 patients with chronic parenchymatous renal disease and in 32 subjects with primary hypertension. The ouabain-sensitive 42K+ influx was reduced in subjects with chronic renal disease by about 20%, even when they were normotensive. The reduction in these patients was greater than that in patients with essential hypertension. The changes in 42K+ influx and Na+ content with a decrease in the 42K+ influx/Na+ content ratio suggest an inhibition of the Na+ pump in the patients with chronic renal disease. The inhibition of the Na+ pump may be secondary to the hypervolaemia which we suggest is the initial event leading to renal hypertension.     

Increased renal tubular sodium pump and Na+,K+-adenosine triphosphatase in streptozotocin-diabetic rats

The effects of chronic glucose osmotic diuresis on renal tubular sodium pump and Na+,K+-adenosine triphosphatase (ATPase) activities were studied in chronic streptozotocin-induced diabetic rats. Four to seven weeks after streptozotocin (60 mg/kg i.p.) injection, specific renal Na+,K+-ATPase activity showed a 34.8% increase as compared to the saline-citrate treated controls, whereas the nonspecific Mg++-ATPase was not altered. The concentration of Na+,K+-ATPase, estimated from the maximum [3H]ouabain binding site concentration, also showed a significant increase in the chronic streptozotocin-diabetic rats. To determine further the specificity of this increase in Na+,K+-ATPase, the activity of the sodium pump, estimated from ouabain-sensitive 86Rb uptake, was measured in nonenzymatically isolated renal tubules. Again, a significant (+106.4%) increase in the renal tubular sodium pump activity was observed in the streptozotocin-diabetic rats, whereas the nonspecific, ouabain-insensitive 86Rb uptake was not altered. Neither was there any difference in 86Rb uptake by the isolated renal glomeruli. Thus, it appears that chronic streptozotocin-induced diabetes in rats is associated with a significant increase in renal tubular sodium pump and Na+,K+-ATPase. The latter effects may represent an important physiologic adaptation of the kidneys to maintain electrolyte homeostasis in diabetes.