正常成年人和急性脑血管病患者红细胞膜钠钾ATP酶的研究

正常成年人和急性脑血管病患者红细胞膜钠钾ＡＴＰ酶的研究郭英华，周淑华，赵慧元，韩强，王强，滕继军，韩仲岩采用钠钾ＡＴＰ酶活力试剂盒，用化学比色法分别测定正常成人青、中、老年组（各２０例）的钠钾ＡＴＰ酶活力（以在３７℃每小时每毫克蛋白水解ＡＴＰ产生１μ...     

正常成年人和急性脑血管病患者红细胞膜钠钾ATP酶的研究

正常成年人和急性脑血管病患者红细胞膜钠钾ＡＴＰ酶的研究郭英华，周淑华，赵慧元，韩强，王强，滕继军，韩仲岩采用钠钾ＡＴＰ酶活力试剂盒，用化学比色法分别测定正常成人青、中、老年组（各２０例）的钠钾ＡＴＰ酶活力（以在３７℃每小时每毫克蛋白水解ＡＴＰ产生１μ...     

脑血管病患者血清及红细胞膜唾液酸含量研究

本文测定了３８例脑血管病患者和２６例正常人血清及红细胞膜ＳＡ含量，结果，脑血管病患者血清ＴＳＡ含量明显高于对照组（Ｐ〈０．０１），红细胞膜ＳＡ含量明显低于对照组（Ｐ〈０．０５），且出血量及梗塞灶大小与血清ＴＳＡ呈正相关（Ｐ〈０．０５），与红细胞膜ＳＡ含量呈负相关（Ｐ〈０．０１），恢复期患者的血清ＴＳＡ显著低于急性期（Ｐ〈０．０５），其红细胞膜ＳＡ含量极显著高于急性期患者（Ｐ〈０．０１）。恢复期患者     

强直性肌营养不良症的红细胞膜ATP酶的研究

对13例MyD病人和13例健康人的红细胞膜的Na~+-K~+ATP酶和Ca~(2+)-Mg~(2+)ATP酶进行测定,发现两组的Na~+-K~+ATP酶活力无显著区别,且均可被乌本苷抑制,而MyD组的Ca~(2+)-Mg~(2+)ATP酶活力则高于对照组。证明在MyD中存在膜的缺陷,推测Ca~(2+)-Mg~(2+)ATP酶活力改变与细胞内高钙水平有关。     

红细胞膜胆固醇,磷脂及二者比值在脑血管疾病中的测定研究

本文测定１００例脑血管病患者的ＲＢＣＭ－Ｃｈ，ＲＢＣＭｋ－ＰＬ，ＲＢＣＭ－Ｃｈ／ＲＢＣＭ－ＰＬ比值，结果显示：ＲＢＣＭ－Ｃｈ含量疾病组高于正常对照组，但无显著差别，ＲＢＣＭ－ＰＬ含量低于对照组而二者比值高于对照组均有统计学意义，３项指标中以二者比值改变最明显。病人组ＲＢＣＭ－Ｃｈ含量与血清胆固醇含量之间没有相关性。结果表明脑血管病人有红细胞膜脂质含量异常，它与脂质代谢异常和血液高凝状态等病理情况有     

脑梗塞患者红细胞膜ATP酶活性与膜脂质相关性研究

本文对５１例急性脑梗塞，１２例脑动脉硬化症患者和５１例健康人的红细胞膜ＡＴＰ酶活性、脂质含量以及红细胞变形能力进行了测定和相关研究，发现急性脑梗塞患者的红细胞变形能力下降，Ｎａ＋－Ｋ＋ＡＴＰ酶及Ｃ＋＋－Ｍｇ＋＋ＡＴＰ酶活性降低，膜胆固醇含量增高，胆固醇与磷脂比值升高；ＡＴＰ酶活性与红细胞滤过指数（ＩＦ）、胆固醇及胆固醇与磷脂比值呈明显负相关，而与膜磷脂含量呈正相关。脑动脉硬化患者酶活性、膜脂质与磷脂比值和红细胞变形性与对照组相差显著。提示缺血性卒中患者存在着能量代谢障碍，脂质成份改变，且在卒中发生前就有不同程度的改变。因此，治疗脑动脉硬化对预防卒中具有积极意义。     

急性脑梗塞病人的红细胞膜ATP酶活性变化和自由基损伤

测定33例急性脑梗塞病人的红细胞膜Na~ K~-ATP酶和Ca~(2 )Mg~(2 )-ATP酶活性及血浆MDA含量,红细胞SOD活性,与29例正常老年人作比较,发现急性脑梗塞病人的红细胞膜Na~ K~ -ATP酶和Ca~(2 )Mg~(2 )-ATP酶活性均降低,而血浆MDA含量升高,红细胞SOD活性下降。说明急性脑梗塞病人存在红细胞功能受损和自由基损害。这些变化的研究,对于进一步探讨脑梗塞的病理生理及其防治可能具有重要意义。     

大鼠脑损伤后红细胞膜ATP酶活性的变化及意义

选取雄性ＳＤ大鼠８２只，以落体撞击致右顶脑挫裂伤，生化法检测伤后６、２４、７２及１６８ｈ（各时间点１０只）红细胞膜ＡＴＰ酶活性。结果，红细胞膜Ｎａ＋－Ｋ＋－ＡＴＰ酶，Ｃａ＋＋－ＡＴＰ酶活性在伤后６ｈ已明显下降，伤后２４ｈ分别降至０．１０３±０．０４３和０．１０１±０．０７０μｍｏｌＰｉ／ｍｇ蛋白·ｈ，与正常对照组（０．１９４±０．０３０、０．１９８±０．０１９ＵｍｏｌＰｉ／ｍｇ蛋白·ｈ）相比差异显著（Ｐ＜０．００１）。随ＡＴＰ酶活性的抑制，伴有红细胞Ｎａ＋、Ｃａ＋＋含量明显升高和红细胞变形能力的显著降低。提示脑损伤后红细膜ＡＴＰ酶抑制是发生高粘滞血症的原因之一。     

Effects of high-dose methylprednisolone on Na+-K+ ATPase and lipid peroxidation after experimental subarachnoid hemorrhage

The production of oxygen-free radicals and their subsequent peroxidative action on membrane unsaturated fatty acids could be enhanced after subarachnoid hemorrhage. High-dose methylprednisolone (30 mg/Kg i.v.) treatment can antagonize acute SAH-induced brain hypoperfusion and protect the ultrastructural integrity of endothelial cell membranes. Experimental subarachnoid hemorrhage (SAH) was induced in anesthesized rats by slow injection of 0.3 ml of autologous arterial blood into cisterna magna. Tissue lipid peroxidation, quantified as thiobarbituric acid reactive material (TBAR) and Na(+)-K+ ATPase activity were assayed in three different rat brain areas (cerebral cortex, hippocampus and brain stem) of controls (without any surgical manipulation), sham-operated (0.3 ml. of mock CSF into cisterna magna) and after SAH induction, at 1 h, 6 h and 48 h. Na(+)-K+ ATPase activity decreased in the cerebral cortex at 1 h and 6 h and in brain stem at 1 h after SAH, while the same enzymatic activity was unchanged in the hippocampus. High-dose methyl-prednisolone treatment (started immediately after SAH induction) enhanced the Na(+)-K+ ATPase activity until control levels. There was no significant difference in lipid peroxide content between sham-operated and hemorrhagic animals; however, the injection itself induces a transient increase of TBAR (1 h after injection) and methylprednisolone treatment decreases the products of lipid peroxidation in all brain areas.     

急性脑梗死患者红细胞内外Ca~(2+)、ATP含量及膜Ca~(2+)-Mg~(2+)ATPase活性变化的动态研究

目的　探讨脑梗死 (CI)患者急性期红细胞 (RBC)内外 Ca2 + 、ATP含量及膜 Ca2 + - Mg2 + ATPase活性变化的规律。方法　用 FACS Vantage流式细胞仪检测 30例急性期 CI患者及 2 8名健康对照者 RBC内游离 Ca2 + 浓度 ([Ca2 + ]i)、ATP含量及 RBC膜 Ca2 + - Mg2 + ATPase活性 ,并进行动态观察。结果　 CI组 RBC[Ca2 + ]i较对照组显著升高 (P <0 .0 1) ;而 ATP含量、膜 Ca2 + - Mg2 + ATPase活性均较对照组明显降低 (分别为 P<0 .0 5、P<0 .0 0 1)。上述结果老年组较青年组明显。CI组 RBC[Ca2 + ]i:发病第 1～ 2天即明显升高 ,3～7天最高 ,于 8～ 15天逐渐降至较发病 1～ 2天时稍低水平 ,但仍比对照组高。而 RBC内 ATP含量、膜 Ca2 + -Mg2 + ATPase活性在发病第 1～ 2天即明显下降 ,3～ 4天降至最低值 ,1周后两者均略有回升。 CI患者 RBC[Ca2 + ]i分别与膜 Ca2 + - Mg2 + ATPase、ATP含量呈明显负相关 (r=- 0 .90 4、r=- 0 .978,均 P<0 .0 5 ) ;RBC内 ATP含量与膜 Ca2 + - Mg2 + ATPase活性之间呈正相关 (r=0 .835 ,P<0 .0 5 )。结论　 CI急性期存在 RBC内钙超载 ,RBC内 ATP含量、膜 Ca2 + - Mg2 + ATPase活性也参与了 RBC内钙超载的病理过程 ,且与年龄有关     

老年人急性脑梗塞患者红细胞变形能力与红细胞 ATP 酶活性关系的研究

检测了６０例老年人急性脑梗塞患者的红细胞变形能力（ＥＤ），红细胞ＡＴＰ酶活性和红细胞内离子浓度的变化。结果显示：老年人急性脑梗塞患者红细胞滤过指数（ＥＦＩ）较对照组显著增高（Ｐ＜０．００１）；红细胞Ｎａ＋－Ｋ＋－ＡＴＰ酶活性和Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性明显降低（Ｐ＜０．００１）；红细胞内Ｎａ＋、Ｃａ２＋浓度明显增高（Ｐ＜０．００１），而Ｍｇ２＋浓度明显降低（Ｐ＜０．０１）。脑梗塞患者红细胞ＥＦＩ与Ｎａ＋－Ｋ＋－ＡＴＰ酶、Ｃａ２＋－Ｍｇ２＋－ＡＴＰ酶活性、Ｍｇ２＋浓度呈负相关（ｒ＝－０．５４２、－０．４１７、－０．４３６）（Ｐ＜０．００１）；与红细胞内Ｎａ＋、Ｃａ２＋浓度呈正相关（ｒ＝０．４７３、０．４６６，Ｐ＜０．００１）；提示脑梗塞病人ＥＤ降低与红细胞ＡＴＰ酶活性降低有关。     

缺血性脑卒中患者红细胞膜磷脂组分的改变及其与红细胞流变学的关系

目的探讨缺血性脑卒中患者红细胞膜磷脂各组分的改变及其对红细胞流变功能的影响。方法采用高效液相色谱法对５８例缺血性脑卒中、２３例有脑动脉硬化症状的患者和２６名健康人的红细胞膜磷脂各组分含量进行测定，并同时检测红细胞膜胆固醇含量、膜微粘度及红细胞变形能力。结果缺血性脑卒中患者红细胞膜总磷脂（ＴＰＬ）、磷脂酰胆碱（ＰＣ）、磷脂酰乙醇胺（ＰＥ）含量低于对照组；胆固醇（ＣＨＯ）、胆固醇与总磷脂比值（ＣＨＯ／ＴＰＬ比值）高于对照组；红细胞膜流动性、红细胞变形能力降低。直线相关分析，ＰＣ与红细胞膜微粘度、红细胞滤过指数呈负相关；ＰＥ与红细胞膜微粘度呈负相关；神经鞘磷脂（ＳＭ）与红细胞膜微粘度呈正相关。有脑动脉硬化症状的患者红细胞变形能力降低，膜胆固醇、胆固醇与总磷脂比值升高，但膜总磷脂及磷脂各组分无明显改变。结论缺血性脑卒中患者红细胞膜存在以ＰＣ、ＰＥ变化为主的磷脂代谢障碍，并对红细胞流变特性产生影响。     

The distribution of inside-out and right-side-out erythrocyte membrane vesicles in Duchenne progressive muscular dystrophy

Summary In ten cases of Duchenne muscular dystrophy, the distribution of erythrocyte ghost vesicles in dextran 110 gradient was examined. When compared with controls a greater number of inside-out vesicles was observed. It is suggested that the tendency to form abnormally oriented vesicles could result from structural abnormalities of the erythrocyte membranes.

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Zusammenfassung In zehn Fällen von Duchennescher Muskeldystrophie wurde die Verteilung der Erythrozytenschattenvesikel in Dextran 110 untersucht. Verglichen mit Kontrollfällen fand sich bei Duchennescher Muskeldystrophie ein größerer Anteil von Innenseite-Außenvesikeln. Es wird vermutet, daß diese Tendenz, abnorm gerichtete Vesikeln zu bilden, Ausdruck einer strukturellen Anomalie der Erythrozytenmembran sein könnte.

     

The role of Na+‐K+‐ATPase in the epileptic brain

Na+‐K+‐ATPase, a P‐type ATP‐powered ion transporter on cell membrane, plays a vital role in cellular excitability. Cellular hyperexcitability, accompanied by hypersynchronous firing, is an important basis for seizures/epilepsy. An increasing number of studies point to a significant contribution of Na+‐K+‐ATPase to epilepsy, although discordant results exist. In this review, we comprehensively summarize the structure and physiological function of Na+‐K+‐ATPase in the central nervous system and critically evaluate the role of Na+‐K+‐ATPase in the epileptic brain. Importantly, we further provide perspectives on some possible research directions and discuss its potential as a therapeutic target for the treatment of epilepsy.     

脑梗塞患者局部脑血流与红细胞膜微粘度关系的研究

检测了５３例脑梗塞患者及３０例健康对照者的局部脑血流（ｒＣＢＦ）和红细胞膜微粘度（ＥＭ－ＭＶ）。结果显示：患者组患侧半球ｒＣＢＦ与健康组同侧半球比较有极显著性差异（Ｐ＜０．００１）。患者组ＥＭＭＶ与健康对照组比较，明显高于对照组（Ｐ＜０．０１）。ＥＭＭＶ与ｒＣＢＦ呈反比，血液粘度越高，对血流切变应力影响越大，脑血流量越低。提示血液流变学的改变是影响脑血流的重要因素，故降低红细胞膜微粘度，对于改善脑血流量，预防和治疗脑梗塞是十分重要的。     

Channel-mediated and carrier-mediated uptake of K+ into cultured ovine oligodendrocytes

Uptake of radioactive K+ by mature ovine oligodendrocytes (OLGs) maintained in primary culture was measured under steady-state conditions, i.e., in cells maintained in a normal tissue culture medium (5.4 mM K+), and in cells after depletion of intracellular K+ to less than 15% of its normal value by pre-incubation in K(+)-free medium. The latter value is dominated by an active, carrier-mediated uptake (although it may include some diffusional uptake), whereas the former, in addition to active uptake, also reflects passive K+ diffusion through ion selective channels and possible self-exchange between extracellular and intracellular K+, which may be carrier-mediated. The total uptake rate was 144 +/- 10 nmol/min/mg protein, and the uptake after K+ depletion was 60 +/- 2 nmol/min/mg protein, much lower rates than previously observed in astrocytes. The uptake into K(+)-depleted cells was inhibited by about 80% in the presence of ouabain (1 mM) and about 30% in the presence of furosemide (2 mM). Activators of protein kinase C (phorbol esters) and cAMP-dependent protein kinase (forskolin) have been shown to alter the myelinogenic metabolism as well as outward K+ current in cultured OLGs. The present study demonstrates that K+ homeostasis in OLGs is modulated through similar second messenger pathways. Active uptake was inhibited by about 60% in the presence of active phorbol esters (100 nM) but was not affected by forskolin (100 nM). Forskolin likewise had no effect on total uptake, whereas phorbol esters caused a much larger inhibition than expected from their effect on carrier-mediated uptake alone, suggesting that channel-mediated uptake was also reduced.(ABSTRACT TRUNCATED AT 250 WORDS)