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。     

糖尿病患者红细胞膜磷脂成分与Na~＋－K~＋－ATP酶活性的变化

探讨了ＮＩＤＤＭ患者红细胞膜磷脂成分与Ｎａ＋－Ｋ＋－ＡＴＰ酶活性的变化。结果：ＮＩＤＤＭ患者红细胞膜甘油磷脂及神经鞘磷脂显著降低，溶血磷脂酰胆碱显著增高；红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶及Ｍｇ＋＋－ＡＴＰ酶活性降低，且红细胞膜磷脂成分改变与酶活性降低显著相关。提示ＮＩＤＤＭ患者红细胞膜磷脂成分改变对膜Ｎａ＋－Ｋ＋－ＡＴＰ酶与Ｍｇ＋＋－ＡＴＰ酶活性有明显影响，并且它们都可能参与糖尿病视网膜病变的发生。     

高血压腔隙性脑梗塞患者红细胞形态和ATP酶活性的变化

目的探讨红细胞ＡＴＰ酶活性与红细胞形态改变及对高血压并发腔隙性脑梗塞的影响。方法用电镜扫描方法观察３３例高血压及２０例高血压伴腔隙性脑梗塞患者的红细胞形态，并用激光衍射方法及沈茂星法分别测定红细胞变形性及红细胞膜ＡＴＰ酶活性。结果（１）高血压腔梗组口形、嵴形、类球形等异常形态红细胞检出率明显高于高血压组和正常对照组（４．８４±１．６７／２．０４±１．１２／１．４０±０．３３，Ｐ＜０．０１）。（２）高血压腔梗组异常红细胞检出率＞４％者明显高于高血压组（８０％／９．１％，Ｐ＜０．００１）。（３）高血压腔梗组红细胞最大变形指数（ＤＩｍａｘ）及综合变形指数（ＩＤＩ）均低于正常组（Ｐ＜０．０５）。（４）高血压腔梗组及高血压组红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶活性与Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性（μｍｏｌ·ｇＨｂ－１·２ｈ－１），均明显低于正常对照组（Ｐ＜０．０１）。结论高血压患者红细胞膜ＡＴＰ酶活性降低的同时红细胞几何形态出现异常，并伴有红细胞变形性减低，是腔隙性脑梗塞的原因之一。因此，高血压的防治除降压，抗血小板等治疗外，还应给予改善ＡＴＰ酶活性，促使红细胞形态正常化的治疗，以防止梗塞性并发症的发生     

周期性麻痹患者红细胞膜Na~＋－K~＋－ATP酶活性研究

周期性麻痹患者红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶活性研究刘好文田成林卢振敏卞德和李娜胡富清刘俊艳王世彤通过对周期性麻痹患者红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶的测定，发现其活性高于正常人，现报道如下。资料与方法病人３０例中低钾性周期性麻痹（低钾组）患者１６例，...     

原发性高血压Ca^2＋—ATP酶活性改变及光量子治疗对其影响

测定了３０例原发性高血压和３０例正常对照组红细胞膜Ｃａ＾２＋－ＡＴＰ酶活性，并用光量子治疗原发性高血压后观察其红细胞膜Ｃａ＾２＋－ＡＴＰ酶活性改变。结果：高血压病组红细胞膜Ｃａ＾２＋－ＡＴＰ酶活性较对照组降低（Ｐ〈０．０１），而经光量子治疗血压下降后，Ｃａ＾２＋－ＡＴＰ酶活性明显升高（Ｐ〈０．０１）。提示Ｃａ＾２＋－ＡＴＰ酶活性降低可能为原发性高血压的发病机制之一，而光量子治疗高血压的机制可能与其     

慢性肾功能衰竭患者红细胞变形能力与红细胞ATP酶活性及离子浓度…

检测６５例ＣＲＦ患者ＥＤ和红细胞ＡＴＰ酶活性离子浓度的变化。结果显示；ＣＲＦ患者红细胞滤过指数和Ｃａ＾２＋，Ｎａ＾＋明显高于对照组，而Ｎａ＾＋、Ｋ＾＋－ＡＴＰ酶Ｃａ＾２＋－Ｍｇ＾２＋－ＡＴＰ酶活性和Ｋ＾＋、Ｍｇ＾２＋明显低于对照组。ＣＲＦ患者ＩＦ与Ｎａ＾＋－Ｋ＾＋－ＡＴＰ酶、Ｃａ＾２＋－Ｍｇ＾２＋－ＡＴＰ酶活性和Ｋ＾＋、Ｍｇ＾２＋浓度呈负相关，与Ｃａ＾２＋、Ｎａ＾＋浓度呈相关。     

卡托普利对NIDDM微白蛋白尿患者红细胞膜ATP酶活力和红细胞内离子水平的影响

测定２０例正常人及２０例ＮＩＤＤＭ伴微白蛋白尿患者红细胞膜ＡＴＰ酶活力和红细胞内Ｎａ＋、Ｋ＋、Ｃａ＋浓度。结果与正常组比较，ＮＩＤＤＭ微白蛋白尿患者Ｎａ＋－Ｋ＋－ＡＴＰ酶和Ｃａ＋＋－ＡＴＰ酶活力降低（Ｐ＜０．０５和Ｐ＜０．０１）；红细胞内Ｋ＋浓度降低（Ｐ＜０．０５），Ｎａ＋和Ｃａ＋＋浓度增高（Ｐ均＜０．０１）。给予ＮＩＤＤＭ微白蛋白尿患者卡托普利（１２．５ｍｇ，ｔｉｄ，×２周；２５ｍｇ，ｔｉｄ，×１４周）治疗１６周，红细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶及Ｃａ＋＋－ＡＴＰ酶活力和红细胞内Ｎａ＋、Ｋ＋、Ｃａ＋＋浓度基本恢复正常，尿白蛋白排泄量减少。     

慢性肾功能衰竭患者红细胞变形能力与红细胞ATP酶活性及离子浓度关系的研究

检测６５例ＣＲＦ患者ＥＤ和红细胞ＡＴＰ酶活性及离子浓度的变化。结果显示：ＣＲＦ患者红细胞滤过指数（ＩＦ）和Ｃａ２＋，Ｎａ＋明显高于对照组（Ｐ＜０．００１），而Ｎａ＋－Ｋ＋－ＡＴＰ酶、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性和Ｋ＋，Ｍｇ２＋明显低于对照组（Ｐ＜０．００１）。ＣＲＦ患者ＩＦ与Ｎａ＋－Ｋ＋－ＡＴＰ酶、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性和Ｋ＋、Ｍｇ２＋浓度呈负相关，与Ｃａ２＋、Ｎａ＋浓度呈正相关。提示ＣＲＦ患者ＥＤ降低与红细胞ＡＴＰ酶活性降低和离子浓度异常有关。     

胆固醇,甘油三醇,高密度脂蛋白与红细胞膜离子酶活性关系研究

目的 探讨高血压旱血浆胆固醇,甘油三酯（ＴＧ）和高密度脂蛋白（ＨＤＬ－Ｃ０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Ｃａ＾２＋、ＡＴＰ酶活性,膜Ｃ／Ｐ克分子比率及膜内面Ｃａ＾２＋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Ｈ     

血压持续偏高青少年红细胞内离子浓度及膜ATP酶活性的变化观察

我们测定了３８例血压持续偏高青少年红细胞膜ＡＴＰ酶活性和红细胞内阳离子浓度。结果表明：Ｎａ＾＋－Ｋ＾＋－ＡＴＰａｓｅ和Ｃａ＾２＋－Ｍｇ＾２＋－ＡＴＰａｓｅ活性明显低于血压正常青少年。红细胞钠、钙含量，红细胞内游离钙水平均明显高于血压正常者。提示：青少年期血压持续偏高个体已存在细胞内钙、钙离子水平的改变，Ｎａ＾＋０Ｋ＾＋－ＡＴＰａｓｅ和Ｃａ＾２＋－Ｍｇ＾２＋ＡＴＰａｓｅ活性降低是血压持续偏高的重要环     

Na~+-K~+-ATP酶活性与缺血半暗带脑组织缺血再灌注损伤的研究

目的探讨Na+-K+-ATP酶活性与缺血半暗带(IP)脑组织再灌注损伤的关系。方法 75只雄性Wistar大鼠随机分为假手术组15只,模型组60只。模型组又根据缺血再灌注时间分为6、24、48及72h4个时间点,每个时间点15只。模型组采用线栓法制备缺血2h再灌注模型。2组大鼠分别于再灌注6、24、48、72h断头取脑,观察IP脑组织Na+-K+-ATP酶活性、神经症状评分、脑组织水肿程度及脑梗死范围的变化。结果与假手术组比较,模型组大鼠IP脑组织Na+-K+-ATP酶活性明显降低(P<0.05),大鼠神经症状评分、脑组织含水量及脑梗死面积明显升高(P<0.05)。随着缺血再灌注时间的延长,大鼠神经症状评分、脑组织含水量均在48h升至最高,IP脑组织Na+-K+-ATP酶活性在48h降至最低,脑梗死面积在72h达最大值。结论在IP脑组织缺血再灌注损伤过程中,Na+-K+-ATP酶活性的改变起着至关重要的作用。     

饮水型砷中毒致人体红细胞膜Na^＋-K^＋-ATP酶活性的改变及膜损伤

目的探讨饮水型砷中毒致人体红细胞膜Na^＋-K^＋-ATP酶活性的改变,并用扫描电镜观察膜的损害。方法对45例不同程度砷中毒患者（病例组）、84例病区内对照（内对照组）、58例病区外对照（外对照组）抽取抗凝血,分离血清,采用分光光度法分别测定各组细胞膜Na^＋-K^＋-ATP酶活性,用扫描电镜观察各组红细胞膜形态的改变。结果（1）病例组Na^＋-K^＋-ATP酶活性（1．89±0．76）u／mg prot,内对照组Na^＋-K^＋-ATP酶活性（2．76±1．27）u／mg prot,外对照组Na^＋-K^＋-ATP酶活性（3．65±1．31）u／mg prot,3组酶活性比较,外对照组、内对照组、病例组酶活性依次降低（P〈0．05）;（2）轻度病例组Na^＋-K^＋-ATP酶活性（1．97±0．75）u／mg prot,中度病例组Na^＋-K^＋-ATP酶活性（1．80±0．79）u／mg prot,重度病例组Na^＋-K^＋-ATP酶活性（1．26±0．87）u／mg prot,3组酶活性比较,差异无统计学意义（P〉0．05）;（3）扫描电镜观察内对照非地方性砷中毒患者和轻中重度地方性砷中毒病人的红细胞膜形态均发生了变形,且膜的受损程度与病人病情相一致。结论饮水型砷中毒可导致红细胞Na^＋-K^＋-ATP酶活性的降低及膜损伤。     

脑梗死患者血浆组织型纤溶酶原激活物和抑制物活性的变化及意义

为了探讨动脉硬化性脑梗死患者急性期和恢复期的组织型纤溶酶原激活物及其抑制物活性的变化及其意义,采用发色底物法检测9例脑梗死患者和40例健康老年人的血浆组织型纤溶酶原激活物和抑制物1活性.对脑梗死患者的梗死体积和神经功能缺损进行了计算和评分,结果发现,脑梗死组急性期和恢复期的组织型纤溶酶原激活物活性分别为0.26±0.14和0.21±0.11 kIU/L,显著低于健康组(P<0.01);纤溶酶原激活物抑制物1活性分别为0.90±0.25和0.98±0.12 kAU/L,显著高于健康组(P<0.01);脑梗死体积为8.75±1.21 cm3;急性期神经功能缺损评分为18.56±3.62;组织型纤溶酶原激活物活性与脑梗死体积和神经功能缺损程度负相关(r=-0.5133,JP<0.05;r=-0.4914,P<0.05),纤溶酶原激活物抑制物1活性与脑梗死体积和神经功能缺损程度正相关(r=0.5621,P<0.05;r=0.5342,P<0.05)。结果提示,脑梗死患者急性和恢复期血浆纤溶活性显著降低,提示组织型纤溶酶原激活物与抑制物1在动脉硬化性脑梗死的病理过程中发挥了重要的作用。     

Alterations of Na+-K+-ATPase, Ca2+-ATPase, and Mg2+-ATPase activities in erythrocyte, muscle, and liver of traumatic and septic patients

Na+-K+-ATPase, Ca2+-ATPase and Mg2+-ATPase activities of erythrocyte membrane, microsomal fractions of rectus muscle, and liver were measured colorimetrically in the biopsy specimens of 14 control, 7 uncomplicated trauma (group 2), and 14 severe trauma or septic patients (groups 3-A and 3-B). In erythrocytes, these three ATPase activities in group 2 were not significantly changed but sepsis of both the acute (group 3-A) and ongoing type (group 3-B) decreased all of the ATPase activities. In muscle, there was a significant loss of three ATPase activities in the acute insult of severe trauma or sepsis (group 3-A), while Na+-K+-ATPase and Mg2+-ATPase activities were not significantly changed in ongoing, severe trauma (group 3-B). In the liver, a tendency for all three ATPase activities to decrease is noted in the severe traumatic group. However, a statistical difference between the control and severe traumatic group showed only for Na+-K+ ATPase and Mg2+-ATPase in group 3-A and Ca2+-ATPase in group 3-B. Correlation coefficients between erythrocyte, muscle, and liver for three ATPase activities are between 0.4 and 0.5. The mechanism which alters ATPase activity remains unknown in this study, but it may account for the variation in traumatic insult, in hemodynamic and hormone changes, and in tissue energy stores.     

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.     

A family of hereditary stomatocytosis associated with normal level of Na+-K+-ATPase activity of red blood cells

A rare familial case of hereditary stomatocytosis with hemolytic anemia, increased autohemolysis, increased osmotic fragility, and shortened erythrocyte survival is described. The erythrocytes were abnormally permeable to sodium and potassium. In addition, "Na-K pump" rate of the red blood cells was increased, while Na+-K+-ATPase, Mg2+-ATPase and Mg2+-Ca2+-ATPase activities were within normal limits. Splenectomy induced marked improvement of anemia.     

IDDM患者红细胞膜Na~＋－K~＋－ATPase活性变化及相关研究

对２０例ＩＤＤＭ患者红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ活性变化及其与红细胞内Ｎａ＋、Ｋ＋浓度、红细胞变形指数（ＥＦＩ）、空腹血糖、年龄、病程的关系进行了分析。结果表明ＩＤＤＭ患者红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰａｓｅ活性明显下降，且与红细胞内Ｎａ＋浓度、ＥＦＩ、病程呈负相关，而与空腹血糖、年龄无相关性。提示红细胞膜Ｎａ￣＋－Ｋ￣＋－ＡＴＰａｓｅ活性改变对红细胞变形能力有影响。     

Salt intake and sensitivity of intestinal and renal Na+-K+ atpase to inhibition by dopamine in spontaneous hypertensive and Wistar-Kyoto rats

The present study evaluated the activity of jejunal Na+-K+-ATPase and its sensitivity to inhibition by dopamine in spontaneous hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats during low (LS), normal (NS) and high (HS) salt intake. Basal jejunal Na+-K+-ATPase activity in SHR on LS intake was higher than in WKY rats. Jejunal Na+-K+-ATPase activity in WKY rats, but not in SHR, on LS intake was significantly reduced (20% decrease) by dopamine (1 microM) and SKF 38393 (10 nM), but not quinerolane (10 nM), this being antagonized the D1 receptor antagonist (SKF 83566). Changing from LS to NS or HS intake in WKY rats increased basal jejunal Na+-K+-ATPase activity and attenuated the inhibitory effect of dopamine. In SHR, changing from LS to NS or HS intake increased basal jejunal Na+-K+-ATPase activity. Basal renal Na+-K+-ATPase activity in SHR on LS intake was similar to that in WKY rats and was insensitive to inhibition by dopamine. Changing from LS to NS or HS intake in WKY rats increased basal renal Na+-K+-ATPase activity without affecting the inhibitory effect of dopamine. In SHR, changing from LS to NS or HS intake failed to alter basal renal Na+-K+-ATPase activity. It is concluded that inhibition of jejunal Na+-K+ ATPase activity by D1 dopamine receptor activation is dependent on salt intake in WKY rats, and SHR animals fail to respond to dopamine, irrespective of their salt intake.     

Prolactin stimulates Na+-K+-ATPase activity located in the outer renal medulla of the rat

The effect of rat prolactin on rat renal Na+-K+-ATPase activity was investigated by a cytochemical technique. Rat prolactin caused stimulation of Na+-K+-ATPase activity only in the outer medulla of the kidney, and not in renal cortical structures. Peak enzyme activity in cultured rat renal segments occurred after tissue had been exposed to rat prolactin for 2 min, and the time of maximal stimulation did not vary with the concentration of prolactin. There was a curvilinear response in Na+-K+-ATPase activity over the rat prolactin concentration range, 0.04-40 ng/l, but higher prolactin concentrations caused inhibition of enzyme activity. Na+-K+-ATPase response was totally blocked by specific rat prolactin antiserum. Human prolactin had no consistent effect on rat medullary Na+-K+-ATPase activity. Addition of specific tri-iodothyronine and arginine vasopressin antisera to rat prolactin was without effect, confirming that the stimulatory action of rat prolactin on Na+-K+-ATPase was not due to contamination with these hormones which are known to stimulate this enzyme.