硫酸铜络合法测定枸橼酸钾含量

目的:确定测定枸橼酸钾缓释片中枸橼酸钾含量的方法.方法:利用枸橼酸盐与Cu2+的络合物在紫外区有特定吸收,测定枸橼酸钾缓释片中枸橼酸钾的含量.结果:枸橼酸钾与硫酸铜形成络合物时最大摩尔比为1:1,枸橼酸钾浓度在10.78～53.9 ug/ml范围内,测定波长为(240±2)nm,吸收度与浓度呈良好线性关系,平均回收率为98.1%,RSD=1.85%(n=9).结论:方法、简单、准确,可作为枸橼酸钾缓释片中枸橼酸钾含量测定方法.     

示波极谱滴定法测定植物中钾含量的研究

示波极谱滴定法测定植物中的钾未见报道,本文用示波极谱滴定法对植物中钾的测定,做了多方面的研究。实验表明以HAc-NaAc为底液pH＝5.0的缓冲溶液中,加入过量的标准四苯研究钠(Na-TPB)溶液,然后用标准AfNO3溶液滴定过量的四苯硼钠,利用四苯硼钠示波极谱曲线(dE／dt＝f(E))上有切口,并和Ag+能定量反应,使切口消失为终点。测定结果满意。该法直观、简便、快速、灵敏、准确、不用加指示剂。溶液混浊、沉淀及有色,均不干扰测定, 适用于植物中钾的测定。     

示波极谱滴定法测定植物中钾含量的研究

示波极谱滴定法测定植物中的钾未见报道,本文用示波极谱滴定法对植物中钾的测定,做了多方面的研究。实验表明以ＨＡｃ－ＮａＡｃ为底液ｐＨ＝５．０的缓冲溶液中,加入过量的标准四苯研究钠（Ｎａ－ＴＰＢ）溶液,然后用标准ＡｆＮＯ３溶液滴定过量的四苯硼钠,利用四苯硼钠示波极谱曲线（ｄＥ／ｄｔ＝ｆ（Ｅ））上有切口,并和Ａｇ＋能定量反应,使切口消失为终点。测定结果满意。该法直观、简便、快速、灵敏、准确、不用加指示剂。溶液混浊、沉淀及有色,均不干扰测定,适用于植物中钾的测定。     

土壤中钾细菌的筛选及筛选底物加入量对其数量的影响

研究土壤中加入不同数量的钾长石粉后其解钾细菌数量的变化,同时初步筛选钾细菌,为进一步研究土壤中解钾细菌的分离、筛选及其鉴定提供参考。测试土壤中加入不同数量的钾长石粉后其解钾细菌数量,对结果进行比较分析;利用四苯硼钠法测试菌株解钾能力,并进行初步筛选。结果表明,按钾细菌数量由多到少的顺序,筛选底物加入量为0.2%0.1%0.4%空白对照;筛选菌株的解钾效率高于K01的共14株,高于K02的共9株。解钾效率最高的菌株5.15-2解钾效率为35.4%,较外购生产菌种K01高13倍,与本实验室保存菌种K02相比高3.6倍。     

HERG钾通道在细胞容量调节中的作用

目的:研究HERG钾通道在细胞容量调节中的作用,并探讨其作用机制。方法:全部试验应用稳定转染HERG-HEK293细胞和HEK293细胞。应用全细胞膜片钳技术记录HERG钾电流。结果:1当HERG-HEK293细胞处于低渗状态,指令电压为0 mV时,Istep增加60%(n=12,P0.05);如指令电压为+30 mV,Itail增加72.1%(n=11,P0.01),增大的HERG电流可被特异性HERG钾电流阻断剂Cisapride(100nM)抑制,Istep被抑制97.2%(n=6,P0.01),Itail被抑制174.1%(n=6,P0.01)。2在低渗状态,指令电压为0 mV时,容量调节性氯通道阻断剂尼氟灭酸(NFA,10 nmol/L)使Istep抑制46.2%(n=12,P0.01),Itail抑制48.5%(n=11,P0.01);给以容量调节性氯通道阻断剂DIDS 100μmol/L时,Istep抑制45.9%(n=12,P0.01),Itail抑制51.1%(n=11,P0.01)。结论:HERG通道部分参与调节性细胞容量下降过程。其参与的细胞容量调节与容量调节性氯通道的激活相伴随。     

土壤中缓效钾测定方法的前处理改进与探讨

根据《土壤速效钾和缓效钾的测定》（NY/T 889-2004）要求,测定土壤中缓效钾可采用热硝酸浸提-油浴消解法来获得酸性钾的含量,用该含量减去速效钾含量就能得到缓效钾的含量,此方法的结果虽然可靠,但前处理方法仍存在一些缺点。对此,文章研究并探讨了有效测定土壤中缓效钾含量的方法,笔者经过多次尝试改进前处理方法,使检测过程操作简单,能节省时间,适用于大批样品的分析测试。     

改进AccQ.Tag法快速测定9R复合氨基酸和3H支链氨基酸注射液中氨基酸含量

应用改进的 A cc Q.Tag法测定 9R复合氨基酸注射液和 3H支链氨基酸注射液中氨基酸含量 ,仅用 9m in就可快速分离测定。经与标准 Acc Q .Tag法测定结果比较 ,该法准确、快速 ,具有很好的实用性     

钙离子激动钾通道在大鼠逼尿肌不稳定膀胱中的表达及变化

目的:探讨钙离子激动钾通道与逼尿肌功能变化之间的关系.方法:根据膀胱压力容积测定结果将动物分为稳定组(29只)和不稳定组(9只),其中稳定组分为BOO(11只)、SCI模型(9只)和时照组(9只),通过RT-PCR技术测定逼尿肌中各型钙离子激动钾通道表达及变化.结果:正常大鼠中逼尿肌不稳定发生率为24.3%.钙离子激动钾通道BKCa和SKCa亚型在各组模型大鼠逼尿肌中均有表达.钙离子激动钾通道BKCa亚型在IDI组、BOO和SCI组逼尿肌中的表达低于正常对照组.结论:钙离子激动钾通道的表达异常引起平滑肌细胞静息电位降低、兴奋性增高可能是引起逼尿肌不稳定的原因之一.     

长期定位施肥对保护地土壤供钾特性的影响

研究了16年定位施肥条件下,不同施肥方式对蔬菜保护地土壤中有效钾含量与土壤供钾特性的影响。结果表明:土壤全钾含量保持在较高水平22.43～26.92g.kg-1;与不施有机肥处理相比,长期施用有机肥后土壤全钾含量有所下降(单施磷肥处理除外),但不同的化肥单施或配施对土壤全钾含量影响不大;长期单施或化学肥料配施土壤的供钾强度和钾素有效率都不高,但施用有机肥明显提高了土壤有效钾含量及土壤的供钾能力,其中,长期单施化学钾肥土壤中有效钾含量为195.60mg.kg-1,单施有机肥处理为460.14mg.kg-1,而化学钾肥与有机肥配施后增长为621.06mg.kg-1;土壤供钾强度和钾素有效率在施用有机肥后也大幅度提高。     

菜豆根瘤菌对土壤钾的活化作用

以土壤为钾源,通过液体培养试验研究了8株菜豆根瘤菌对土壤钾的活化作用。结果表明,菜豆根瘤菌能释放大量的氢离子,使液体培养基的pH值大幅度降低,氢离子的浓度至少提高22倍以上。根瘤菌分泌有机酸的种类与数量因菌株不同而异,这些有机酸包括甲酸、乙酸、草酸、丁二酸、柠檬酸、苹果酸和乳酸等,其中全部菌株均能分泌草酸和苹果酸,大部分菌株能分泌乙酸。在接种根瘤菌的液体培养基中,可溶性钾含量显著高于不接种的液体培养基,土壤矿物结构钾则显著降低。由于土壤是培养基钾的唯一来源,故根瘤菌可促进土壤无效钾的溶解。相关分析表明,土壤矿物结构钾与有机酸分泌总量呈极显著负相关(r=-0.878**,n=9),与培养液pH值呈极显著正相关(r=0.863**,n=9),说明根瘤菌分泌的有机酸和氢离子可能溶解土壤无效钾。考虑到根瘤菌草酸分泌量大,络合钙、镁、铁、铝的能力强,且与有机酸分泌总量呈极显著正相关(r=0.870**,n=9),推测草酸分泌在活化土壤无效钾的过程中起重要作用。此外,根瘤菌分泌的有机酸电离产生的氢离子仅占培养液氢离子的4.15%—27.56%,推测根瘤菌直接分泌的氢离子可能是造成培养液pH值降低的主要原因之一。     

Active sodium and potassium transport in high potassium and low potassium sheep red cells

The kinetic characteristics of the ouabain-sensitive (Na + K) transport system (pump) of high potassium (HK) and low potassium (LK) sheep red cells have been investigated. In sodium medium, the curve relating pump rate to external K is sigmoid with half maximal stimulation (K_1/2) occurring at 3 mM for both cell types, the maximum pump rate in HK cells being about four times that in LK cells. In sodium-free media, both HK and LK pumps are adequately described by the Michaelis-Menten equation, but the K_1/2 for HK cells is 0.6 ± 0.1 mM K, while that for LK is 0.2 ± 0.05 mM K. When the internal Na and K content of the cells was varied by the PCMBS method, it was found that the pump rate of HK cells showed a gradual increase from zero at very low internal Na to a maximum when internal K was reduced to nearly zero (100% Na). In LK cells, on the other hand, no pump activity was detected if Na constituted less than 70% of the total (Na + K) in the cell. Increasing Na from 70 to nearly 100% of the internal cation composition, however, resulted in an exponential increase in pump rate in these cells to about ⅙ the maximum rate observed in HK cells. While changes in internal composition altered the pump rate at saturating concentrations of external K, it had no effect on the apparent affinity of the pumps for external K. These results lead us to conclude that the individual pump sites in the HK and LK sheep red cell membranes must be different. Moreover, we believe that these data contribute significantly to defining the types of mechanism which can account for the kinetic characteristics of (Na + K) transport in sheep red cells and perhaps in other systems.     

Brain tissue potassium in normal and potassium depleted rats

The potassium concentration of muscle, brainstem and diencephalon were studied in normal and potassium-depleted rats. With 13% depletion of muscle potassium there was a 2.1% and 2.8% decrease in brainstem and diencephalon tissue potassium respectively. With 34% depletion of muscle potassium there was a 1.9% and 4.0% decrease in brainstem and diencephalon tissue potassium. These small decreases in regional brain tissue potassium could be related to observed functional alterations in the potassium depleted rat, i.e., altered cerebrospinal fluid bicarbonate regulation and altered control of the pattern of breathing and of body temperature regulation.     

Basolateral K-Cl cotransporter regulates colonic potassium absorption in potassium depletion

Active potassium absorption in the rat distal colon is electroneutral, Na(+)-independent, partially chloride-dependent, and energized by an apical membrane H,K-ATPase. Both dietary sodium and dietary potassium depletion substantially increase active potassium absorption. We have recently reported that sodium depletion up-regulates H,K-ATPase alpha-subunit mRNA and protein expression, whereas potassium depletion up-regulates H,K-ATPase beta-subunit mRNA and protein expression. Because overall potassium absorption is non-conductive, K-Cl cotransport (KCC) at the basolateral membrane may also be involved in potassium absorption. Although KCC1 has not been cloned from the colon, we established, in Northern blot analysis with mRNA from the rat distal colon using rabbit kidney KCC1 cDNA as a probe, the presence of an expected size mRNA in the rat colon. This KCC1 mRNA is substantially increased by potassium depletion but only minimally by sodium depletion. KCC1-specific antibody identified a 155-kDa protein in rat colonic basolateral membrane. Potassium depletion but not sodium depletion resulted in an increase in KCC1 protein expression in basolateral membrane. The increase of colonic KCC1 mRNA abundance and KCC1 protein expression in potassium depletion of the rat colonic basolateral membrane suggests that K-Cl cotransporter: 1) is involved in transepithelial potassium absorption and 2) regulates the increase in potassium absorption induced by dietary potassium depletion. We conclude that active potassium absorption in the rat distal colon involves the coordinated regulation of both apical membrane H,K-ATPase and basolateral membrane KCC1 protein.     

Clinical potassium problems

Alterations in serum potassium are common in many diseases. In a series of 390 determinations of serum potassium, the levels found were low in 24 per cent and high in 2.6 per cent. The major causes of low serum potassium are (1) decreased potassium intake due to intravenous feedings which do not contain potassium; (2) increased loss of potassium in the urine due to accelerated tissue breakdown, or renal lesions; (3) loss from the gastrointestinal tract due to diarrhea, or fistulae, and (4) shift between serum and cells, due to metabolic causes, drugs or changes in pH. The major cause of high serum potassium is uremia with renal retention.Clinical symptoms and signs of low body potassium include muscle weakness and paralysis, which may lead to death in respiratory failure if not corrected, tachycardia, gallop rhythm, dilatation of the heart. The electrocardiogram shows inverted, low amplitude, or isoelectric T waves and a prolonged QT interval. Potassium chloride orally, subcutaneously or intravenously is recommended for use in the treatment of potassium deficits. It should not be used in the presence of oliguria or anuria or dehydration. The amounts of potassium necessary to correct deficits vary widely and cannot be predicted from the serum level. Special reference is made to the prevention and therapy of potassium deficits in diabetic acidosis. High serum potassium levels are difficult to correct. Suggested measures are administration of glucose, insulin or calcium, gastric or peritoneal lavage or use of the artificial kidney.     

Fixation of proteins by osmium tetroxide potassium dichromate and potassium permanganate

Summary The crosslinking abilities of osmium tetroxide, potassium dichromate and potassium permanganate towards bovine serum albumin and bovine -globulin were investigated by chromatography with Sephadex G-200. Osmium tetroxide had a moderate crosslinking ability towards these proteins, the others had little or none. Chromatography with Sephadex G-50 permitted the oxidative cleavage of the proteins by these oxidative fixation agents to be studied. Potassium permanganate caused much fragmentation of the proteins and destruction of the tyrosine and tryptophan residues. Osmium tetroxide and potassium dichromate caused only a small amount of protein cleavage. These results were corroborated by polyacrylamide gel electrophoresis and viscosimetric studies. The significance of the results for tissue fixation is discussed.