利多卡因对家兔心肌缺血／再灌注损伤Na^＋-K^＋-ATPase、Ca^2＋ -Mg^2＋ -ATPase及NO的作用

目的:研究利多卡因对心肌缺血/再灌注损伤家兔心肌Na -K -ATPase、Ca2 -Mg2 -ATPase及血清NO的影响。方法:24只家兔随机分为3组:假手术组(A组)、缺血/再灌注组(B组)、利多卡因组(C组),每组8只。B组、C组阻断左冠状动脉前降支40 min,再灌注90 min,A组仅穿线不结扎。C组于开放冠状动脉再灌注前经颈静脉注射利多卡因5 mg/kg,A、B组注射等量生理盐水。于再灌注90min取颈静脉血测定NO。再灌注90 min后取心肌组织测定NOS、Na -K -ATPase、Ca2 -Mg2 -ATPase。结果:心肌组织Ca2 -Mg2 -ATPaseB组较A、C组降低(P<0.01);Na -K -ATPase B组较A、C组降低(P<0.01);血清NO、心肌组织NOS:B组较A、C组降低(P<0.01)。结论:利多卡因对心肌缺血/再灌注损伤具有保护作用。     

原发性高血压肾病患者红细胞ATP酶活性检测的临床意义

目的 探讨原发性高血压肾病患者红细胞膜Na^＋、K^＋-ATP酶活性的改变参与原发性高血压肾病的可能机制。方法 按Reilni制膜法测定32例原发性高血压无肾病和40例原发性高血压肾病患者红细胞膜Na^＋、K^＋-ATP酶和Ca^2＋、Mg^2＋-ATP酶含量,并与35名正常健康人作比较。结果 原发性高血压无肾病组和肾病组细胞膜Na^＋、K＋-ATP酶和Ca^2＋、Mg^2＋-ATP酶活性均显著地低于正常人组（P〈0.01）。原发性高血压肾病组与无肾病组亦有显著性差异（P〈0.05）。结论 原发性高血压肾病的发生和发展与细胞膜Na^＋、K^＋-ATP酶和Ca^2＋、Mg^2＋-ATP的活性有密切的关系。     

地奥心血康对大鼠心肌缺血再灌注损伤防护机制的探讨

目的观察地奥心血康（DK）对大鼠心肌缺血再灌注损伤的影响。方法40只Wistar大白鼠随机分为正常对照组、模型对照组，每日灌胃0．5％羧甲基纤维素钠10ml／kg，与DK给药组，每日灌胃DK70mg／kg，共10d。结扎大鼠冠状动脉左前降支30min，再灌注90min后复制出大鼠心肌缺血再灌注损伤模型，观察心肌梗死面积、心肌Na^＋ - K^＋ ATP酶、Ca^2＋ - ATP酶、超氧化物歧化酶（SOD）、过氧化氢酶（CAT）、谷胱甘肽过氧化物酶（GSH-Px）和丙二醛（MDA）等的变化。结果与模型对照组相比DK给药组心肌梗死面积明显缩小，Na^＋ - K^＋ ATP酶、Ca^2＋ - ATP酶、SOD、CAT及GSH-Px显著升高、MDA显著降低（P〈0．05，P〈0．01）。结论DK对大鼠心肌缺血再灌注损伤有保护作用。其机制可能与清除自由基，保护心肌Na^＋ - K^＋ ATP酶、Ca^2＋ - ATP酶免受自由基破坏有关。     

缺血预处理减轻心肌缺血再灌注诱导的Na+-K+-ATP酶异常表达

目的：探讨Na^＋ -K^＋ -ATP酶在心肌缺血预处理保护机制中的作用。方法：以前降支结扎30min后复灌60min制备心肌缺血再灌注模型，连续3次缺血5min再灌注10min制备缺血预处理模型。以毛花甙丙抑制Na^＋ -K^＋ -ATP酶功能，观察心脏收缩和舒张功能、心肌Na^＋ -K^＋ -ATP酶功能，免疫组化法检测Na^＋ -K^＋ -ATPα1、α2、α3及β1亚基的蛋白表达。结果：心肌缺血再灌注显著抑制心脏舒缩功能、Na^＋ -K^＋ -ATP酶活性以及α1、α2、α3及β1亚基的蛋白原位表达；缺血预处理可减轻心肌缺血再灌注诱导的Na^＋ -K^＋ -ATP酶异常，保护心脏功能；毛花甙丙可维持心脏舒缩功能，但显著抑制Na^＋ -K^＋ -ATP酶和蛋白表达。结论：缺血预处理能减轻心肌缺血再灌注诱导的Na^＋ -K^＋ -ATP酶异常，抑制Na^＋ -K^＋ -ATP酶功能导致缺血预处理保护作用丧失，维持Na^＋ -K^＋ -ATP酶功能是缺血预处理心肌保护重要机制之一。     

右旋美托咪定后处理对大鼠心肌缺血再灌注损伤的保护作用

目的：评价右旋美托咪定（DEX）后处理对大鼠心肌缺血再灌注时Na⁺-K⁺-ATP酶和Ca²⁺-ATP酶活性的影响。方法：36个成年雄性Wistar大鼠心脏置于改良的Langendoff装置上,均为平衡灌注末HR>180次/min、左室收缩压>75mm Hg、室性早搏<2个/min的心脏模型,采用随机数字表法分为3组：对照组（A组）、缺血再灌注组（B组）、DEX处理组（C组）,每组12个。A组持续灌注KH液180 min,B组和C组在KH平衡灌注20 min时常温停灌40 min后恢复灌注,于再灌注即刻分别灌注KH液、含100 nmol·L^-1 DEX的KH液20 min,然后继续再灌注KH液100 min。监测心率（HR）、冠状动脉流出量（CF）,左心室发展压（LVDP）、左心室内压最大上升和下降速率（±dP/dt_max）,采用酶联免疫法测定心肌Na⁺-K⁺-ATP酶、Ca²⁺-ATP酶,以梗死心肌质量占心室质量的百分比表示心肌梗死率。结果：再灌注后A组心功能优于B组、C组（P<0.05）,C组优于B组（P<0.05）。与A组比较,B组和C组心肌梗死率较大,心肌组织Na⁺-K⁺-ATP酶、Ca²⁺-ATP酶的活性降低（P<0.05）;与B组比较,C组心肌梗死率低,心肌组织Na⁺-K⁺-ATP酶、Ca²⁺-ATP酶的活性较高（P<0.05）。结论：DEX后处理可提高Na⁺-K⁺-ATP酶和Ca²⁺-ATP酶的活性,减轻大鼠心肌缺血再灌注损伤。     

安氟醚麻醉下牵拉胆囊对心肌ATP酶、ET、NOS的影响

目的 研究安氟醚麻醉下牵拉胆囊对心肌ATP酶、ET、NOS的影响。方法 健康家兔24只，随机分为A、B、C三组，A组对照组，B组吸入安氟醚达0．65MAC，C组吸入安氟醚达1．3MAC。暴露胆囊，坠以100g重物牵引10分钟。迅速开胸，取心肌组织测定ATP酶、内皮素(ET)、一氟化氯合成酶(NOS)。结果 三组心肌细胞的Na^2 —K^ ATPase、Mg^2 -ATPase差异元显著性，C组的Ca^2 -ATPase明显低于A组(P＜0．05)，B组、C组的ET明显低于A组(P＜0．05)。结论 安氟醚麻醉下牵拉胆囊可抑制了心肌细胞Ca^2 -ATPase和ET的释放。     

青龙衣多糖对H22型肿瘤细胞的ATPase活性影响的研究

目的 研究青龙衣多糖对H22型肿瘤细胞的ATPase活性的影响。方法 按照测定无机磷含量的方法对H22肿瘤细胞的Ca^2＋-ATPase、Na^＋K^＋-ATPase和Mg^2＋-ATPase活性进行了测定。结果 发现青龙衣多糖可以降低ATPase的活性，除青龙衣多糖中、高剂量组显著抑制Ca^2＋-ATPase活性。高、中、低剂量组都显著降低Na^＋-K^＋-ATPase和Mg^2＋-ATPase活性（P〈0．05）。结论 ATPase活性降低导致了膜电位下降。细胞容积降低．可能引起细胞凋亡发生．Ca^2＋．调节凋亡发生．Mg^2＋调控ATPase的活性,可能是青龙衣多糖抗肿瘤的机制之一。     

线粒体及内质网对铅引起的[Ca2+]i升高的作用

目的 研究线粒体、内质网Ca^2 -ATP酶以及Na^ 和K^ -ATP酶活力的改变对铅引起的[Ca^2 ]i升高的调节作用，探讨铅引起的[Ca^2 ]i增高对学习记忆功能的影响。方法 Wistar大鼠神经肉瘤C6细胞培养于含醋酸铅的培养液中，于不同时间终止染铅，检测[ca2’]；及线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力。结果 (1)0．2μmol／L染铅组：[Ca^2 ]i轻度升高，线粒体Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力升高，内质网酶活力略增高；(2)1．0μmol／L染铅组：[Ca^2 ]；于染铅后0．5h升至最高，以后逐渐降低，波动于iL60～190nmol／L之间；线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶于染铅后0．5h升至最高(分别为未染铅前酶活力的29．1、39．2、10．8和19．8倍)，2d后降至接近正常水平。结论 (1)铅可使Wistar大鼠神经肉瘤C6细胞Ca^2 浓度及线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力增高；(2)当[Ca^2 ]i增高不显著时以线粒体Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力增高为主；当[Ca^2 ]i急剧升高时，线粒体、内质网Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力均明显增高，尤其是线粒体Ca^2 -ATP酶、Na^ 和K^ -ATP酶活力增高更为显著。     

芦荟苷预处理对缺血再灌注大鼠心肌细胞凋亡、TNF-α含量和Ca2+-ATPase活性的影响

摘要：目的研究芦荟苷（Barbaloin,Barb）对急性心肌缺血再灌注损伤大鼠心肌细胞凋亡的影响。方法结扎大鼠左冠状动脉前降支复制心肌缺血再灌注损伤模型,实验分为假手术组、缺血再灌注组（IR）、Barb高、低剂量预处理组。采用原位缺口末端标记法（TUNEL）检测心肌细胞凋亡指数（AI）,ELISA法测定血清TNF—α水平,化学法测定线粒体Ca^2＋-ATPase活性。结果与IR组比较,Barb组AI和TNF-α水平显著降低（P〈0．05或P〈0．01）,Ca^2＋-ATPase活性明显增高（P〈0．05）。结论Barb能明显抑制IR引起的心肌细胞凋亡,其作用可能与降低TNF-α水平和提高Ca2＋-ATPase活性有关。     

自体血液回收技术对红细胞膜ATP酶的影响

目的 探讨血液回收技术对红细胞膜Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性的影响。方法 将24例患者麻醉前静脉血、术野回收原血及回收红细胞血液标本采用沈茂星法测定红细胞膜Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性,并予统计分析。结果 经血液回收技术处理后的红细胞膜Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性与术野回收血值比较均有显著降低（P〈0．05）。结论 自体血液回收技术能使红细胞膜Na^＋-K^＋-ATP酶和Ca^2＋-Mg^2＋-ATP酶活性明显降低。     

Effects of calcium antagonists on (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities of rat cortical synaptosomes

1. The effects of 11 calcium antagonists on (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities of rat cortical synaptosomes were studied. 2. All the calcium antagonists studied had inhibitory effects on ouabain-sensitive (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities in synaptosomes at high concentrations (10 or 100 microM). 3. Calcium antagonists such as trifluoperazine, flunarizine and cinnarizine had inhibitory effects on Ca2+-ATPase activity at low concentrations (1-10 microM). 4. Trifluoperazine and La3+ had inhibitory effects on Mg2+-ATPase activity at low concentration (1 microM). 5. Our results suggest that most of the calcium antagonists studied have little effects on neuronal (Na+ + K+)-ATPase, Mg2+-ATPase and Ca2+-ATPase activities at therapeutic dose ranges (1 microM or lower).     

Chronic digoxin treatment on canine myocardial Na+, K+-ATPase

Summary In order to determine whether a prolonged inhibition of cardiac Na⁺, K⁺-ATPase causes a compensatory or adaptive change in this enzyme, the relationships among serum digoxin concentration, binding of digoxin to the enzyme and cardiac Na⁺, K⁺-ATPase and sodium pump activity were studied in dogs chronically treated with digoxin. Digoxin was injected intravenously twice daily up to 4 weeks. Two hours after the injection of a single non-toxic dose of digoxin, Na⁺, K⁺-ATPase and sodium pump activities were inhibited quantitatively in a manner corresponding to the binding of digoxin to the enzyme. The magnitude of sodium pump inhibition was reduced 12 h after the digoxin injection, with simultaneous decreases in serum digoxin concentration and the binding of digoxin to the enzyme. After 1 or 4 weeks of digoxin treatment with non-toxic doses, the relationships among serum digoxin concentration, binding of digoxin to cardiac Na⁺, K⁺-ATPase and the degree of cardiac Na⁺, K⁺-ATPase or sodium pump inhibition remained unchanged. The magnitude of the inhibition was related to serum digoxin concentrations and digoxin binding to cardiac Na⁺, K⁺-ATPase, in a manner similar to that observed after a single digoxin injection. After 4 weeks of digoxin treatment with toxic doses, these relationships were also unaffected. It was concluded that prolonged digoxin treatment fails to alter the inhibition of myocardial Na⁺, K⁺-ATPase by this agent.This work was supported by U.S. Public Health Service Grant HL-16052.     

bFGF对慢性酒精中毒大鼠肝组织ATP酶活力的影响

目的 观察碱性成纤维细胞生长因子(bFGF)对慢性酒精中毒大鼠肝组织Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力的影响,探讨bFGF对慢性酒精中毒所致的肝损伤的保护作用.方法 选择成年Wistar雄性大鼠,采用白酒灌胃建立慢性酒精中毒模型,慢性酒精中毒模型建立成功的大鼠随机抽签法分为酒精中毒对照组、生理盐水(NS)对照组和bFGF治疗组.另10只不灌白酒作为正常对照组.bFGF治疗组大鼠白酒灌胃的同时,1h后按12μg/kg剂量肌肉注射,共14d.各组大鼠到相对应的时间点取出肝组织制成匀浆,测定肝组织匀浆中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力.结果 与正常对照组相比,慢性酒精中毒后大鼠肝组织中Na+-K+-ATF酶活力及Ca2+-Mg2+-ATP酶活力均明显降低(P<0.05);经bFGF治疗后肝组织中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显高于酒精中毒对照组及NS对照组(P<0.05).结论 bFGF能提高慢性酒精中毒肝组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力,提示bFGF对慢性酒精中毒所致的肝损伤具有保护作用.     

复合离子盐对老年人细胞内Na+、K+、Ca2+的影响及其机制

目的：观察复合离子盐对老年人细胞内Na^＋、K^＋、Ca^2＋及红细胞膜钠泵和钙泵活性的影响。方法：在天津市河东区社区中抽取226例老年人作为研究对象．其中高血压者112例。正常血压者114例。两者再随机分为离子盐组和普通加碘盐组．分别给予复合离子盐和普通加碘盐摄入，6个月后观察研究对象细胞内Na^＋、K^＋、Ca^2＋及钠泵、钙泵活性的变化。结果：6个月时高血压患者中离子盐组细胞内钠、钙离子浓度低于基线水平（P〈0．05），但钾离子无明显变化。离子盐组钠泵、钙泵活性均明显高于基线水平（P〈0．05），但在正常血压者中，2组与基线水平比较差异无统计学意义。结论：复合离子盐可增强钠泵、钙泵活性，使细胞内的钠、钙含量减少。     

Inhibition of human erythrocyte Ca2+-ATPase by Zn2+.

Recent investigations suggest that Ca2(+)-ATPase from fish gills is very sensitive to Zn2+ (Hogstrand et al., 1996. Am. J. Physiol. 270, R1141-R1147). The effect of free Zn2+ ion on the human erythrocyte plasma membrane Ca2(+)-ATPase was investigated to explore the possible extension of this finding to humans. Membrane vesicles were prepared and the Ca2(+)-ATPase activity was measured as Ca2(+)-stimulated ATP hydrolysis and as ATP-dependent Ca2+ transport. The Zn2+ ion inhibited the erythrocyte Ca2(+)-ATPase by reducing Vmax and increasing the K0.5. While in the Ca2+ transport assay only the Vmax was affected at lower Zn2+ concentrations (50-100 pM), reduction of Vmax was always accompanied by an affinity decrease in the ATP hydrolysis assay. The Ca2(+)-ATPase was found to be inhibited by Zn2+ at extremely low concentrations. The IC10 and IC50 for Zn2+, at a Ca2+ concentration of 1.0 microM, were estimated at 4 and 80 pM, respectively. Although the Ca2(+)-ATPase might be more sensitive in vitro than in vivo conditions, the results suggest that physiological concentrations of Zn2+ may reduce the activity of the erythrocyte Ca2(+)-ATPase. Furthermore, disturbance of Ca homeostasis may be a mechanism causing Zn toxicity during exposure.     

Inhibition of the mitochondrial Mg2+-ATPase by propranolol

The in vitro effects of propranolol, a commonly used beta-adrenergic blocker, on the membrane structure and function of rat heart mitochondria were investigated. It was found that the respiratory control and oxidative phosphorylation of the isolated mitochondria decreased concomitantly when the drug was added to the assay medium. At the concentration higher than 1.0 X 10(-4) M, propranolol significantly inhibited the State 3 respiration but had little effect on the State 4 respiration of the mitochondria. On the other hand, the drug exhibited noncompetitive inhibitions toward the Mg2+-ATPase activity of submitochondrial particles and purified enzyme preparations at the concentrations ranging from 3.0 X 10(-4) to 1.5 X 10(-3) M. The inhibitory constants of propranolol toward the enzyme activity in submitochondrial particles and in the purified preparation were estimated to be 6.7 X 10(-4) and 1.4 X 10(-3) M, respectively. However, the drug did not show significant effect on the activity of any of the enzyme complexes of the mitochondrial respiratory chain. It is thus concluded that propranolol impairs the mitochondrial respiration and oxidative phosphorylation mainly through its inhibition of the Mg2+-ATPase activity of the mitochondria. This effect of propranolol may explain, at least partly, its depression effects on the cardiac functions of the animal.