老年糖尿病患者红细胞膜Na+-K+-ATP酶活性及临床意义

通过测定老年糖尿病患者龚细胞膜Ｎａ＾＋－Ｋ＾＋－ＡＴＰ酶活性,发现糖尿病患者红细胞Ｎａ＾＋－Ｋ＾＋－ＡＴＰ酶活性明显低于对照组,糖尿病伴神经病变患者神经传导速度明显减慢,Ｎａ＾＋－Ｋ＋－ＡＴＰ酶活性倾向低于不伴神经病变者。     

血清Na~+浓度对慢性乙型重型肝炎患者预后的评价作用

目的分析慢性乙型重型肝炎患者的血清Na+浓度与预后的关系,比较血清Na+水平、MELD-Na评分与凝血酶原时间(PT)对慢性乙型重型肝炎患者短期预后的预测价值。方法慢性乙型重型肝炎患者85例,分成生存组和死亡组,分别记录患者入院第2天的血清Na+、MELD-Na评分和PT,并分析三者之间的相关性;运用受试者工作特征曲线(ROC)及曲线下面积(AUC)评价血清Na+、MELD-Na评分和PT的预测价值。结果生存组患者血清Na+、MELD-Na评分值和PT分别为136.08±5.66mmol/L,20.42±7.78和22.28±6.37s,死亡组患者血清Na+、MELD-Na分值和PT分别为131.15±6.97mmol/L、34.40±10.72和34.48±10.09s,三项指标均有显著性差异,P0.001。血清Na+与MELD-Na评分值呈显著负相关(r=-0.673,P0.001),血清Na+与PT亦呈负相关(r=-0.238,P0.05),血清Na+浓度、MELD-Na分值和PT的AUC分别为0.261、0.878和0.870。结论低钠血症是影响慢性乙型重型肝炎预后的重要因素,包含血清Na+的MELD-Na评分与PT均能较好地预测慢性乙型重型肝炎患者的短期预后,两者预测能力无显著差异。     

血清胆碱脂酶测定对重型肝炎患者的临床意义

目前公认:早发现、早防治,是重型肝炎提高存活率的关键。血清胆碱脂酶(cholinesterase,ChE)主要由肝细胞合成,肝脏炎症时其活力降低,故可作为判断肝功能状况的良好指标。为了解ChE对重型肝炎患者临床诊治和监护的意义,我们作了如下观察。 1 资料与方法 1.1 资料 随机采集我院1997～1998年住院的30例重型肝炎患者,其中慢性重型肝炎者15例,亚急性重型肝炎者10例,肝功能衰竭者5例。重型肝炎的临床诊断按1995年5月(北京)第5届全国病毒性肝炎会议修订的诊断标准。     

D-α-生育酚调节蛋白激酶C活性对糖尿病视网膜病变的影响

目的　探讨蛋白激酶C(PKC)在糖尿病视网膜病变 (DR)中的作用和D α 生育酚对糖尿病视网膜毛细血管组织病理的影响。方法　实验大鼠分为 4组 :正常对照组 (C组 )、D α 生育酚处理的正常对照组 (T组 )、糖尿病组 (D组 )、D α 生育酚处理病鼠组 (DT组 )。血糖、HbA1c和D α 生育酚含量以及原位PKC、ATPase活性在处理后 6个月被检测 ,毛细血管床形态立体定量评估DR。结果病程 6个月时 ,D组大鼠深、浅层毛细血管呈现周细胞减少、基底膜增厚的特征性改变 ,成模 6个月后糖尿病大鼠视网膜PKC活性显著增高 >10 0 % ,D α 生育酚可阻止此升高。同一大鼠视网膜 ,D α 生育酚也可阻止糖尿病诱导的Na+ K+ ATPase和Ca2 + ATPase活力下降。D α 生育酚可显著改善糖尿病视网膜微血管周、内皮细胞截面积和深浅层毛细血管基底膜厚度 ,而对血糖、HbA1c无影响。结论糖尿病诱导的组织病理异常可能大部分由PKC介导 ,D α 生育酚可改善糖尿病视网膜毛细血管超微结构     

重型肝炎时血清甲状腺素变化的临床研究

肝脏参与甲状腺素的代谢,严重肝脏疾患时,血清甲状腺素可出现一些特殊的变化,如急性肝炎时的“高Ｔ４综合征”［１］以及肝硬化时的“低Ｔ３综合征”、“低Ｔ３、Ｔ４综合征”等［２,３］。关于重型肝炎时甲状腺素血清学变化的研究,目前报道较少。我们就此展开探讨,...     

血清胆碱酯酶活性对诊断亚急性乙型重型肝炎的价值探讨

目的　探讨血清胆碱酯酶 (Che)活性对亚急性乙型重型肝炎的诊断价值。方法　常规检测亚急性乙型重型肝炎与急性肝炎患者血清Che活性 ,血清Che活性对亚急性乙型重型肝炎与急性乙型肝炎的鉴别价值分析采用ROC曲线法。结果　亚急性重型肝炎血清Che活性 ( 5 44 7.7± 2 75 9.2 )u/L ,急性肝炎血清Che活性为 110 73 .6± 2 911.7u/L ,两者相比有显著性差异 (t =1.984,P =0 .0 0 0 )。鉴别亚急性重型肝炎与急性肝炎的血清Che活性的ROC曲线下面积0 .915 ,显著大于标准参考线下面积 (P =0 .0 0 0 )。以血清Che活性≥ 75 48u/L诊断急性肝炎而排除亚急性重型肝炎的灵敏度、特异度和准确度分别为 0 .883、0 .88和 0 .882 ,阳性和阴性预测值分别为 0 .95 8和 0 .710 ,阳性和阴性似然比分别为7.3 5 8和 0 .13 3。结论　血清Che活性测定对排除亚急性重型肝炎有比较可靠的预测价值     

替米沙坦对OK细胞Na^＋-K^＋ATP酶活性的影响

目的　探讨血管紧张素Ⅱ受体拮抗剂 (ARB)替米沙坦和血管紧张素转换酶抑制剂 (ACEI)苯那普利对负鼠近端小管上皮细胞 (OK细胞 )Na+ K+ ATP酶活性的影响。方法　培养的OK细胞采用低渗方法制备细胞膜悬液 ,使用BCA 1 0 0蛋白质定量测定试剂盒测定膜蛋白 ;Na+ K+ ATP酶活性采用孔雀绿比色分析法测定释放的无机磷 (Pi)含量 ,培养液中分别加入血管紧张素Ⅱ (AngⅡ )、AngⅡ +血管紧张素Ⅱ受体拮抗剂替米沙坦 (Telmisartan)、AngⅡ +血管紧张素转换酶抑制剂苯那普利 (Benazepril) ,观察它们对OK细胞Na+ K+ ATP酶活性的影响。结果　 (1 )培养液中加入 1 0 - 1 0 mol/LAngⅡ组与对照组相比 ,OK细胞Na+ K+ ATP酶活性明显上升。 (0 0 972± 0 0 0 80vs 0 0 896± 0 0 0 65μmol·L- 1 ·mgpro- 1 ·h- 1 ,P <0 0 5) (2 )当培养液中同时加入 1 0 - 1 0 mol/LAngⅡ和 1 0 - 9mol/LTelmisartan ,与单加入 1 0 - 1 0 mol/LAngⅡ组相比 ,OK细胞Na+ K+ ATP酶活性明显降低。 (0 0 62 3± 0 0 0 53vs 0 0 972± 0 0 0 80 μmol·L- 1 ·mgpro- 1 ·h- 1 ,P <0 0 5) (3)当培养液中同时加入 1 0 - 1 0 mol/LAngⅡ和 1 0 - 9mol/LBenazepril,与单加入 1 0 - 1 0 mol/LAngⅡ组相比 ,OK细胞Na+ K+ ATP酶活     

重型肝炎血清γ-谷氨酰转肽酶水平与预后探讨

γ-谷氨酰转肽酶(γ-GT)对肝脏系统疾病的诊断很有价值.为了探讨重型肝炎患者血清γ-GT水平及其与预后的关系,我们对近2年来168例重型肝炎和有重型肝炎倾向患者进行了血清γ-GT含量检测,现将结果报道如下.     

重型肝炎患者血清甲胎蛋白的变化

本文对38例重型肝炎患者甲胎蛋白(AFP)的改变进行分析。资料与方法一、一般资料我科2004—2006年住院的重型肝炎患者38例。男31例,女7例,年龄14~86岁,平均年龄(43.89±17.86)岁。其中急性重型肝炎3例,亚急性重型肝炎12例,慢性重型肝炎23例。乙型肝炎病毒(HBV)血清标志阳性者29例,病原未明6例,甲型肝炎1例,药物性肝损害1例(亚急性),酒精性肝损害1例(重型酒精性肝炎)。住院时间(30.76±27.17)d,最短1d,最长者113d。根据临床转归将患者分为存活组23例,死亡组16例。重型肝炎的诊断符合2000年西安会议修订的标准[1]。药物性肝损害的诊断依据《…     

益气养阴活血对中国小型猪心肌梗死后早期心甲橹疦a+-K+ATP酶、Ca2+-Mg2+ATP酶活性及抗氧化的作用

目的 采用结扎中国小型猪冠状动脉造成急性前壁心肌梗死(AMI)模型,应用益气养阴活血中药(复方芪丹液)干预动物AMI后早期心室重构(VR)的影响,并研究其对动物心肌钙、镁离子和氧自由基的作用.方法 中国小型猪28只,采取结扎冠状动脉左前降支中下1/3部,造成AMI模型.手术成功存活动物随机分为复方芪丹液大、小剂量组及卡托普利(开搏通)组、模型组、假手术组共5组,均予灌胃给药或自来水4周.4周后测定猪的血流动力学指标、心肌Na+-K+ATP酶、Ca2+-Mg2+ATP酶活性、心肌超氧化物歧化酶(SOD)、丙二醛(MDA)含量等.结果 与模型组比较,复方芪丹液大剂量组的左室内压(LVP)、血压(BP)、-dp/dtmax值明显升高(P<0.01),复方芪丹液小剂量组及开博通组LVP显著升高(P<0.05),开博通组-dp/dtmax值显著升高(P<0.05).复方芪丹液大剂量组Na+-K+ATP酶、Ca2+-Mg2+ATP含量较模型组显著升高(P<0.05),复方芪丹液小剂量组、开博通组与模型组相比Ca2+-Mg2+ATP酶仅有升高的趋势,未有统计学意义(P>0.05);复方芪丹液大剂量组、复方芪丹液小剂量组、开博通组SOD活力较模型组均显著升高(P<0.05).复方芪丹液大剂量组的MDA含量与模型组比较显著降低(P<0.05).结论 益气养阴活血中药可提高中国小型猪AMI后心肌收缩力,改善血流动力学指标;增加SOD活性,降低MDA含量,提高细胞膜Ca2+-Mg2+ATP酶和Na+-K+ATP酶活力,起到干预AMI后VR和保护心肌的作用.     

Studies on the Na+-K+-ATPase in myocardial infarction

Changes in the cardiac sarcolemma in myocardial infarction were studied by both determination of Na+-K+-ATPase activity and SDS gel electrophoretic analysis of sarcolemmal proteins in the canine heart. Ninety minutes after coronary ligation, Na+-K+-ATPase activity in ischemic myocardium was decreased significantly to approximately 36% of that of non-ischemic myocardium, and it remained at the lower level for 28 days. By SDS gel electrophoresis, reduction of the protein band with molecular weight of 111,000, which is suggestive of the main component of ATPase, was observed simultaneously with the reduction of Na+-K+-ATPase activity. These results indicate that ischemia for 90 minutes produces substructural changes in the sarcolemma indicating irreversible myocardial changes.     

Some Properties of Erythrocyte Na+ -K+ -ATPase in Essenial Hypertension

The activity and some allosteric properties of Na⁺ -K⁺ -ATPase in erythrocytes and their membrane preparations (ghosts) from 57 patients with essential hypertension and 36 normotensive controls were studied. To reveal enzyme activity in whole erythrocytes the cells were pretreated with detergent Tween-20. It was found that in the patient erythrocytes the Na⁺ -K⁺ -ATPase activity was 33% less as compared to the control group. Moreover, in the patient erythmcytes the sensitivity of the enzyme to high concentrations of MgCI₂ was decreased. In contrast, no analogous changes of the enzyme were revealed in the patient ghosts. It is suggested that the erythrocytes of patients with essential hypertension contain an inhibitor of Na⁺ -K⁺ -ATPase.     

Outward Na+-K+-Cl- cotransport function in erythrocytes from essential hypertensives

We have performed a kinetic analysis of the interaction of the outward Na+-K+-Cl- cotransport system with intra-cellular Na+ in erythrocytes from 30 normotensive controls and 72 patients with essential hypertension. Neither maximal rate of ouabain-resistant, bumetanide-sensitive sodium efflux (Vmax) nor intracellular Na+ content required for half-maximal stimulation (K50%) were significantly different between normotensives and hypertensives. Nevertheless, using 95% confidence limits of the K50% in the normotensive group as a cut-off point, 21 (29.17%) essential hypertensive patients exhibited values above the upper normal limit of 20.11 mmol/l cells, revealing a decreased apparent affinity of outward Na+-K+-Cl- cotransport for internal Na+ ('Co-' hypertensives). The Vmax of Na+-K+-Cl- cotransport exhibited a great variability among hypertensives but 'Co-' patients tended to have increased values of this parameter when compared with the remaining essential hypertensives (959 +/- 84 vs 652 +/- 39 mumol/l cells/h, P = 0.0024). Mean BP values were significantly lower in the 'Co-' subset (121.4 +/- 1.6 mmHg), compared with the remaining 51 hypertensive patients (126.4 +/- 1.3 mmHg, P = 0.0297). We conclude that an abnormal function of outward Na+-K+-Cl- cotransport is present in 19% to 40% of Spanish patients with essential hypertension and this abnormality may be implicated in the mechanisms of hypertension.     

Kinetic analysis of erythrocyte Na+-K+ pump and cotransport in essential hypertension

Alterations in red blood cell (RBC) Na+-K+ pump and Na+-K+ cotransport have been described in essential hypertension. We evaluated Na+-K+ pump and cotransport in 30 hypertensive and 26 normotensive subjects subdivided by race and family history of hypertension using an improved method to examine the kinetics of Na and K effluxes. RBCs were Na-loaded by the nystatin method to five different levels of internal Na with pump determined as ouabain-sensitive Na efflux and cotransport as furosemide-sensitive Na and K efflux. Two kinetic parameters were determined for both transport systems: the apparent affinity for Na (K0.5) and the velocity of efflux at saturating internal Na concentration (Vmax). Mean intracellular Na content in fresh RBCs (mmol/L cells) was higher in black hypertensive (12.6 +/- 1.8 mmol/L cells) and normotensive subjects (10.9 +/- 1.2 mmol/L cells) than in white hypertensive (8.7 +/- 1.0 mmol/L cells) or normotensive subjects (8.5 +/- 0.8 mmol/L cells). The Vmax and K0.5 for pump were not significantly different between study groups. The Vmax for cotransport was elevated in white hypertensive compared with normotensive subjects, but the K0.5 values were similar. Black normotensive and hypertensive subjects displayed a lower Vmax and increased K0.5 for cotransport compared with the white groups. A family history of hypertension had no influence on cotransport kinetics in blacks but did predict white normotensive and hypertensive subjects with low cotransport. The reduction in intracellular Na affinity for cotransport in black subjects may explain their higher intracellular Na in fresh RBCs.(ABSTRACT TRUNCATED AT 250 WORDS)     

甲状腺功能减退大鼠心肌抗氧化能力及Na+-K+-ATP酶α1亚基mRNA表达的研究

采用低碘饮食建立甲状腺功能减退(甲减)动物模型,观察心肌抗氧化能力及Na+-K+-ATP酶α1亚基mRNA的变化,结果显示甲减大鼠心肌抗氧化能力下降,导致心肌过氧化损伤,心肌细胞萎缩,心脏内膜软骨化生,膜上参与代谢的ATP酶活性降低,Na+-K+-ATP酶α1亚基mRNA的表达下降.     

内皮素B受体对肾近曲小管上皮细胞Na+-K+-ATP酶活性的影响

目的 探讨内皮素B(ETB)受体对肾脏近曲小管(RPT)上皮细胞Na -K -ATP酶活性的影响和机制.方法 以WKY(Wistar-Kyoto)大鼠RPT细胞为研究对象,Na -K -ATP酶活性采用哇巴因法进行测定.结果 ETB受体激动剂BQ3020能明显降低Na -K -ATP酶的活性,这一抑制作用呈浓度和时间依赖性,BQ3020 10-8 mol/L刺激15 min达最大效应,下降幅度达36.1%;用细胞膜钙通道阻断剂尼卡地平预先刺激细胞后,能够阻断ETB受体对Na -K -ATP酶的抑制效应;在无钙状态下,ETB受体激动剂BQ3020对Na -K -ATP酶的抑制效应丧失.结论 ETB受体在RPT处通过降低Na -K -ATP酶活性调节离子转运;细胞外钙内流参与了ETB受体对Na -K -ATP酶活性抑制作用的信号途径.     

Na+-K+ pump inhibition caused by chronic amiodarone in guinea pig myocardium

Summary Although it is known that amiodarone inhibits myocardial Na⁺-K⁺ pump activity, the potency and the time course of this inhibition are unknown. The aim of this study was to investigate these aspects with reference to digoxin, using guinea pigs treated with either intraperitoneal amiodarone (20mg/kg per week, up to 12 weeks,n = 26) or the same amount of vehicle as a control (n = 24). ECG recording and microelectrode experiments were conducted every 2 weeks. QT interval corrected by heart rate and action potential duration were prolonged as a function of the time of exposure to amiodarone. Hyperpolarization observed immediately after the overdrive (1.0Hz) termination or K⁺-replenishment following K⁺-depletion in the presence of 0.1mM Ba²⁺ was compared in the amiodarone-treated and untreated groups, as an index of the Na⁺-K⁺ pump activity. The resting membrane potential recovery from overdrive-induced depolarization was slower and the amplitude of K⁺-induced hyperpolarization was smaller in the amiodarone-treated group than in the untreated group. These changes were evident as the chronic amiodarone treatment progressed, although the changes in these parameters were greater in the case of acute application of 50µM digoxin. In conclusion, this study indicates that treatment with amiodarone for longer than several weeks moderately inhibits the myocardial Na⁺-K⁺ pump.This work was partly supported by a Grant-in-Aid for Scientific Research from the Ministry of Education, Science and Culture of Japan (11877125).     

Characteristics of Hypertensive Patients With Increased Plasma Na+-K+Pump Inhibitory Activity

Recent studies in our laboratories and in the laboratories of other investigators suggest the presence of a sodium-potassium pump inhibitor in the plasma of some patients with arterial hypertension. We here review these studies in an attempt to determine what characteristics increase the likelihood of detecting the inhibitor. The review suggests but does not prove that the inhibitor is most likely to be found in males with increased sodium intake, decreased renal function, and decreased plasma renin activity. In future studies of plasma sodium-potassium pump inhibitory activity in hypertensive humans, we should pay more attention to the characteristics of the patients. These characteristics include age, sex, race, therapy, stage of hypertension, sodium intake, renal function, and renin status. We should also make an attempt to match the patients properly with normotensive control subjects.