糖尿病患者红细胞钠含量和钠转运

本文测定了50例NIDDM患者和26例正常健康人红细胞钠含量和钠转运。结果表明:糖尿病患者红细胞钠含量明显高于正常人,红细胞钠泵活性明显低于正常人,而糖尿病患者红细胞膜对钠的通透性与正常人差异则无显著性。女性糖尿病患者红细胞钠含量和钠泵活性的变化比男性患者为大。胰岛素在体外能明显降低糖尿病患者红细胞钠含量和升高红细胞钠泵活性。     

卡托普利对高血压病患者红细胞钠和钙离子转运的影响

本文观察了高血压病(EH)患者红细胞膜钠泵、钙泵活性和红细胞内离子浓度的变化,以及卡托普利对其的影响。结果表明,59例EH患者钠泵和钙泵活性显著低于正常人,细胞内钠和钙离子浓度显著高于正常人。其中23例经卡托普利治疗后,钙泵活性升高,细胞内钙离子浓度下降,其升高或减少的程度与血压的下降之间有显著相关性。提示EH患者存在钠和钙离子转运障碍,卡托普利对其有一定影响。     

兔动脉粥样硬化进程中胆固醇,红细胞膜钠泵活性和膜收缩蛋白…

通过喂饲高胆固醇饲料复制家兔主动粥样硬化模型，呈现ＡＳ早期的晚期的变化。在ＡＳ进程中显示：（１）血清总胆固醇浓度呈明显升高趋势；（２）红细胞膜洋活性逐渐降低；（３）红细胞膜收缩蛋白相对含量下降。胆固醇浓度与钠泵活性、ＳＰ含量间分别呈显著或非常显著负相关；钠泵活性ＳＰ含量间呈显著或非常显著正相关。     

糖尿病患者红细胞膜脂质成分改变与膜钠泵K~ -pNPPase活性的关系

对52例非胰岛素依赖型糖尿病(NIDDM)患者红细胞膜脂质成分和膜钠泵K~ -pNPPase(钾激活对硝基苯磷酸酶)活性进行了测定。结果显示,红细胞膜胆固醇、胆固醇/磷脂比值明显升高,膜磷脂和钠泵K~ -pNPPase活性明显降低;膜钠泵K~ -pNPPase活性降低与膜胆固醇、胆固醇/磷脂比值升高呈负相关,而与膜磷脂呈正相关。提示NIDDM患者红细胞膜脂质成分改变和膜钠泵K~ -pNPPase活性降低密切相关。     

左室舒张功能变化与红细胞内离子、红细胞膜钙泵、钠泵类系的探讨

本文应用无创心功能检查,测定49例不同心脏病患者及30例正常人的左室收缩及舒张功能,并同步测定红细胞内离子浓度及红细胞膜钙泵、钠泵活性,结果显示:心脏病组红细胞膜钙泵活性明显低于正常组,以舒张功能异常者更为显著,且舒张功能异常者红细胞内 Ca++浓度显著增高;高血压心脏病和冠心病组红细胞膜钠泵活性下降。提示心脏病组左室舒张功能异常者与细胞内钙超负荷有关。     

地高辛增加心肌收缩力治疗心衰的细胞学机制(96)

<正>有强心作用的地高辛,其药理作用的主要机制是抑制心肌细胞膜上的钾钠ATP酶,进而抑制心肌细胞膜上钠泵的运转,结果使钠泵将心肌细胞外K+打进细胞内的作用,以及将细胞内的Na+打到细胞外的作用减弱,使心肌细胞内的Na+浓度轻度升高。心肌细胞内Na+浓度的这种轻度升高将增加心肌细胞膜上钠钙交换体的活性,使较多的Na+经该交换体打到细胞外,同时交换回更多的Ca2+进入心肌细胞内。     

高血压病病人红细胞变形能力与红细胞膜钙依赖中性蛋白酶活性的关系

目的：探讨高血压病病人红细胞变形能力（ＥＤ）变化与红细胞膜钙依赖中性蛋白酶活性的关系。方法：采用ＥＤ测定仪、分光光度计和凝胶电泳法分别检测了１２６例高血压病病人和６７例健康人红细胞滤过指数、红细胞膜钙依赖中性蛋白酶活性、钙—三磷酸腺苷（Ｃａ２＋－ＡＴＰ）酶活性和红细胞膜收缩蛋白相对含量的变化。结果：高血压病病人红细胞滤过指数，红细胞膜钙依赖中性蛋白酶活性明显增高，Ｃａ２＋－ＡＴＰ酶活性和红细胞膜收缩蛋白相对含量明显降低，与对照组比较差异有极显著性（Ｐ＜０．００１）。且随着病程进展，各指标变化逐渐明显（Ｐ＜０．０１，Ｐ＜０．００１）。高血压病病人红细胞滤过指数与红细胞膜钙依赖中性蛋白酶活性呈正相关（ｒ＝０．６８０，Ｐ＜０．００１），与Ｃａ２＋－ＡＴＰ酶和红细胞膜收缩蛋白含量呈负相关（ｒ＝－０．５７２，－０．６２７，Ｐ＜０．００１）；Ｃａ２＋－ＡＴＰ酶活性和红细胞膜收缩蛋白含量与红细胞膜钙依赖中性蛋白酶活性呈负相关（ｒ＝－０．５２８，－０．６６０，Ｐ＜０．００１）。结论：高血压病病人ＥＤ降低与红细胞膜钙依赖中性蛋白酶活性增高所致的膜蛋白水解和破坏有关。     

高血压病患者盐敏感性应激血压反应与钠代谢

为观察盐敏感者应激血压反应与钠代谢的关系，对３３例Ⅰ、Ⅱ期高血压病患者和２７例血压正常对照者用静脉盐水负荷和速尿缩容相结合的方法确定盐敏感者（ＳＳ），动态观察精神激发、冷加压和运动试验前后血压变化及普通含钠量饮食下红细胞膜钠泵活性（Ｎａ，Ｋ－ＡＴＰ酶）、钠／锂反转运速率（Ｎａ／ＬｉＣＴ）及红细胞钠含量。ＳＳ于精神激发和冷加压试验后血压上升幅度及由峰值恢复到基础状态时间均大于盐不敏感者（ＳＲ）；红细胞钠含量增高，Ｎａ／ＬｉＣＴ增速，Ｎａ，Ｋ－ＡＴＰ酶活性降低；激发试验后平均动脉压上升幅度与红细胞钠含量正相关，与细胞膜Ｎａ，Ｋ－ＡＴＰ酶活性呈负相关。提示，盐敏感者应激血压反应增强与细胞膜钠离子转运障碍相关联。     

慢性心衰病人血细胞内离子变化与血浆内源性类洋地黄物质含量的关系

本文对50例心衰病人外周静脉血淋巴细胞、红细胞内离子含量,血浆 EDLS 和红细胞膜 Na/K ATP 酶活性进行了同步测定和动态观察,结果提示,心衰病人淋巴细胞及红细胞内钾、镁含量显著降低,钠、钙浓度明显升高,且与升高的血浆 EDLS 呈显著相关性。洋地黄治疗会进一步加剧这一过程。     

尿毒症患者红细胞膜泵功能的研究

本文对32例尿毒症及透析治疗患者的红细胞膜Ca~(2+)-Mg~(2+)+ATP酶和Na~+-K~+ATP酶活性及红细胞内钙、钠离子浓度进行同步测定。发现尿毒症患者的Ca~(2+)-Mg~(2+)ATP酶和Na~+-K~+ATP酶活性降低,红细胞内钙、钠浓度升高,经透析治疗2～3个月后,尿毒症患者血清中分子水平降低,Ca~(2+)-Mg~2+AI"P瞎和Na+.K+ATP酶活性恢复.此外,我们还测定了一次血透前后血浆钙及全血离子钙浓度的变化;并将尿毒症组与同期透析治疗组各项指标作了比较,结果发现同期透析治疗患者的膜泵功能明显恢复,血清钙浓度得到纠正.     

高血压病人红细胞ATPase,细胞离子和游离钙的变化

本研究对 39例轻、中度高血压病 (EH)患者 ,通过皂素溶血定磷法测定红细胞ATPase活力 ,原子吸收火焰法测定红细胞离子含量 ,Fura 2 /AM荧光探针测定红细胞 [Ca2 ]i含量 ,并以正常人作对照 ,旨在探讨部分EH的发病机制。结果显示 ,EH组红细胞Ca2 ATPase活力明显降低 ,P <0 .0 1,而Na K ATPase无显著性差异 ,两者之间呈正相关 (r =0 .46 ) ;红细胞Na 和 [Ca2 ] i含量 ,均显著增高 (P <0 .0 1和 0 .0 0 1) ,而细胞K 含量明显降低 ,以致Na /K 比值增大 (均P <0 .0 1)。研究表明 ,EH患者红细胞高Na ,高 [Ca2 ] i及低K ,是膜缺陷及阳离子转运异常的标志或结果 ,是部分EH患者发病的病理基础和分子生物学基础。红细胞Na 泵活力正常 ,Ca2 泵活力抑制 ,可为EH的一种临床类型     

Platelet and erythrocyte Mg2+, Ca2+, Na+, K+ and cell membrane adenosine triphosphatase activity in essential hypertension in blacks.

OBJECTIVE: To assess the relationship between intracellular Mg2+, Ca2+, Na+ and K+ and cell membrane adenosine triphosphatase (ATPase) activity in normotensive and hypertensive blacks. DESIGN: Intracellular cations and cell membrane ATPase activity were studied in black patients with untreated essential hypertension and age-, weight- and height-matched normotensive controls. Platelet, erythrocyte and serum Mg2+, Ca2+, Na+ and K+ levels as well as platelet and erythrocyte membrane Na+,K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase activities were measured in all subjects. METHODS: Intracellular Na+ and K+ were measured by flame photometry and Mg+ and Ca+ by atomic absorption spectrophotometry. Cell membrane ATPase activity was determined by a colorimetric method. RESULTS: The hypertensive group consistently demonstrated depressed activity of each ATPase studied, with significantly lower serum Mg2+, serum K+, erythrocyte Mg2+ and platelet Mg2+ levels compared with the normotensive group. Platelet Na+ and Ca2+ and erythrocyte Ca2+ were significantly elevated in the hypertensive group. In the hypertensive group, mean arterial pressure (MAP) was inversely correlated with platelet and erythrocyte membrane Na+,K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase. Serum Mg2+, serum Ca2+ and platelet Mg2+ were negatively correlated with MAP in the hypertensive group whilst erythrocyte and platelet Ca2+ were positively correlated. In the normotensive group, platelet Mg2+ and MAP were negatively, and erythrocyte Ca2+ and MAP, positively correlated. CONCLUSIONS: Black patients with essential hypertension have widespread depression of cell membrane Na+,K(+)-ATPase, Ca(2+)-ATPase and Mg(2+)-ATPase activities with serum and intracellular Mg2+ depletion and cytosolic Na+ and Ca2+ overload, which may reflect an underlying membrane abnormality in essential hypertension. These cellular abnormalities may be related to the defective transport mechanisms that in turn may be aggravated by Mg2+ depletion.     

临界高血压转归与红细胞内Na~＋及血浆内源性洋地黄样物质的关系

目的：探讨临界高血压转归与细胞内Ｎａ＋、Ｋ＋及血浆内源性洋地黄样物质（ＥＤＬＳ）的关系。方法：对汉中市心血管病防治区１１０例年龄３０～６０岁临界高血压患者及１０６例血压正常对照组随访１１年，此期间测定了红细胞Ｎａ＋、Ｋ＋（火焰光度法）及血浆内源性洋地黄样物质（地高辛免疫法）含量。结果：经１１年随访，临界高血压转归为确诊高血压者占３０．９％，而对照组仅占４．０％（Ｐ＜０．０１）；临界高血压转归为确诊高血压者与其它各转归组比较，红细胞Ｎａ＋、血浆内源性洋黄样物质含量显著偏高，而红细胞Ｋ＋明显偏低（Ｐ＜０．０１或Ｐ＜０．０５）；红细胞Ｎａ＋、血浆内源性洋地黄样物质偏高者，以后演变为确诊高血压的危险性增大（ＲＲ＝１．９６及３．０７）。结论：临界高血压转归与细胞内Ｎａ＋、Ｋ＋及血浆内源性洋地黄样物质有关，Ｎａ＋、内源性洋地黄样物质增高对临界高血压的转归具有预测意义。     

Role of membrane-bound calcium in the changes of ion permeability and Na+, 5+ and ATPase activity of the erythrocytes in hypertension]

The content of calcium bound to the erythrocyte membrane and the effect of intracellular calcium concentration on the activity of Na+, K+-ATPase in the reconstituted erythrocytes were studied in 20 patients with essential hypertension and in 20 individuals with normal pressure. In incubation of the erythrocytes in a solution containing EDTA much more calcium is removed from the outer surface of their membrane in patients with essential hypertension than in the control group (60 +/- 5 mEq/l and 41 +/- 3 mEq/l, respectively). When the intracellular calcium concentration varies from 0 to 500 mumol/l, which corresponds to a rise in the free calcium (Ca2f+-3) concentration to 41 mumol/l, a difference in the changes of Na+, K+-ATPase activity of the reconstituted erythrocytes is noted. When intracellular calcium concentration is 50 mumol/l (Ca2f+-3 mumol/l), ATP-ase activity in patients with essential hypertension is 21% less than that in individuals with normal pressure (P less than 0.005). The authors explain the difference in the kinetics of Na+, K+-ATPase changes by the different degree of calcium depletion of the inner surface of the erythrocyte membrane in relatively low Ca2f+ values in the internal medium. The data obtained are evidence of the altered calcium-binding capacity of the erythrocyte membrane, which may cause the increased permeability of the erythrocyte membrane to sodium and potassium ions in patients with essential hypertension, which the authors had revealed earlier. The authors consider the revealed changes to be a fragment of a more extensive membrane defect which may be the principal cause of activation of the servomechanisms which maintain arterial pressure.     

高血压病并发脑梗死患者红细胞变形性及细胞膜ATP酶活性的研究

目的：研究高血压病（EH）及并发脑梗死（HCI）患红细胞变形性（RCD）及细胞膜ATP酶活性的改变,方法：采用粘度法,化学比色法测定了20例正常人,30例EH及30例HCI患的红细胞变形指数（DI）,红细胞膜Na^ ,K^ -ATP酶和Ca2 -ATP酶的活性。结果：（1）EH组与正常对照组相比,DI值显升高,ATP酶活性降低,EH患DI与ATP酶活性呈负相关,与DBP呈正相关;（2）CHI组与EH组相比,DI显升高,ATP酶活性显降低;HCI患DI与ATP酶活性呈负相关。结论：（1）EH患RCD降低,并与细胞膜ATP酶活性降低及血压升高相关。（2）RCD降低可能与EH患脑梗死的发生有关。     

胆固醇、甘油三酯、高密度脂蛋白与红细胞膜离子酶活性关系研究

目的探讨高血压时血浆胆固醇（Ｃｈｏ）、甘油三酯（ＴＧ）和高密度脂蛋白（ＨＤＬ－Ｃ）水平与细胞膜离子运输酶活性之间的关系。方法３２名正常人（ＮＴ）,５５例原发性高血压（ＨＴ）患者,检测血浆Ｃｈｏ、ＴＧ、ＨＤＬ－Ｃ水平,红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性,膜Ｃ／Ｐ克分子比率及膜内面Ｃａ２＋结合力。结果（１）ＨＴ组平均动脉血压（ＭＡＰ）与ＮＴ组相比有显著性差别;（２）ＨＴ组血浆ＨＤＬ－Ｃ水平、红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性,以及膜内面Ｃａ２＋结合力均较ＮＴ组明显减低;（３）ＨＴ组血浆Ｃｈｏ,ＴＧ水平、红细胞膜Ｃｈｏ含量和Ｃ／Ｐ克分子比率,与ＮＴ组比较皆明显增高。结论红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶和Ｃａ２＋－ＡＴＰ酶活性减低,以及膜内面Ｃａ２＋结合力减低,是高血压时细胞膜离子运输失常的主要标志,血浆ＴＧ水平升高和膜磷脂水平减低可能是高血压时细胞膜理化特性及离子运输失常的主要决定因素。     

尼莫地平对老年高血压患者内分泌激素和离子转运的影响

目的　探讨血管紧张素Ⅱ (AngⅡ )、去甲肾上腺素 (NE)、内源性类洋地黄物质 (EDLS)和细胞离子转运在老年原发性高血压 (EH)发病及尼莫地平治疗中的作用。方法　测定 2 0例轻中度老年EH患者和 2 1例健康老年人血浆AngⅡ、NE和EDLS及淋巴细胞Na+ 、Ca2 + 转运 ,观察尼莫地平治疗 6个月后各项参数变化。结果　老年EH患者血浆AngⅡ、NE和EDLS升高 ;细胞Na+ K+ 腺苷三磷酸酶 (Na+ K+ ATPase)和Ca2 + 腺苷三磷酸酶 (Ca2 + ATPase)活性降低、Na+ 和Ca2 + 增高、K+ 下降 ;NE与AngⅡ、EDLS、Na+ 和Ca2 + 正相关、与Ca2 + ATPase负相关 ,EDLS与Na+ K+ ATPase负相关。尼莫地平干预后 ,血压、总外周阻力、血浆 3种激素、细胞Na+ 和Ca2 + 降低 ,两种ATPase活性增高。结论　循环内分泌升压激素含量变化和细胞Na+ 、Ca2 + 转运失常及其相互作用可能参与老年EH的发病过程 ;尼莫地平长期治疗 ,能降低老年EH血压并改善其异常的病理生理机制     

The role of endogenous Na+, K(+)-adenosine triphosphatase inhibitory factor in the regulation of membrane fluidity of erythrocytes in essential hypertension.

OBJECTIVE: To investigate the regulatory mechanisms of membrane functions in hypertension, we examined the relationship between endogenous Na+, K(+)-adenosine triphosphatase (ATPase) inhibitor (digitalis-like factor; DLF) and erythrocyte membrane fluidity in essential hypertension by means of an electron spin resonance (ESR) and spin labelling methods. DESIGN AND METHODS: Erythrocytes were obtained from patients with essential hypertension and normotensive subjects, and the ESR spectra for a fatty acid spin label agent (5-nitroxide stearate) incorporated into the erythrocyte membranes were studied. The DLF content in plasma was expressed as the inhibitory potency of dog kidney Na+, K(+)-ATPase activity in vitro. RESULTS: The values of outer hyperfine splitting and of order parameter in ESR spectra were significantly higher in hypertensive patients than in normotensive subjects. This finding shows that the erythrocyte membrane fluidity may be decreased in essential hypertension. The level of plasma DLF content was greater in hypertensive patients than in normotensive subjects and was significantly correlated with the decrease in erythrocyte membrane fluidity. CONCLUSIONS: These results suggest that the decrease in erythrocyte membrane fluidity may be partially dependent upon the increased plasma DLF content.     

胰岛素抵抗在高血压病患者升压机制的探讨

观察了３３例高血压病病人和２５例正常对照者的血糖、胰岛素等生化指标以评价胰岛素敏感性，测定了红细胞胰岛素受体（ＥＩＲ）并分析其与胰岛素敏感性的关系。通过对血浆去甲肾上腺素、醛固酮和红细胞膜上离子泵活力的测定，及血压与上述诸因素的多元回归分析，探讨了高胰岛素血症致ＥＨ的可能机理。结果表明：高血压病人存在胰岛素抵抗（ＩＲ），ＩＲ可能与ＥＩＲ数目减少有关。高胰岛素血症可能是通过增加交感神经活性和醛固酮浓度，改变细胞膜上离子泵等途径致高血压的。     

高血压病患者红细胞变形性改变和细胞膜ATP酶活性对其影响及卡托普利干预

目的 探讨高血压病患红细胞变形性（RCD）改变及细胞膜ATP酶活性对其影响，并观察血管紧张素转换酶抑制剂－卡托普利治疗后的变化。方法 采用粘度法、化学比色法测定了20例正常人、30例高血压病及30例高血压病并发脑梗死患的红细胞变形指数（DI）、红细胞膜Na^ ,K^ -ATP酶和Ca^2 -ATP酶活性。其中30例高血压病患接受卡托普利治疗，共24周。结果（1）高血压病组与正常对照组相比，DI值显升高，ATP酶活性降低；高血压病患DI与ATP酶活性呈负相关，DI与DBP呈正相关。（2）高血压病并发脑梗死组与高血压病组相比，DI显升高，ATP酶活性显降低；高血压病并发脑梗死病患，DI与ATP酶活性呈负相关。（3）卡托普利治疗后DI值显下降，ATP酶活性显升高。结论 （1）高血压病患RCD降低，并与细胞膜ATP酶活性降低及血压升高相关；（2）高血压病患并发脑梗死患RCD较高血压病患更低；（3）卡托普利治疗高血压病患在有效降压的同时，能显增加细胞膜ATP酶活性，增加RCD。