骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶活性在不同训练条件下的变化

背景:Na+,K+-ATP酶和Ca2+-ATP酶存物质运送、能量转换以及信息传递方面具有重要作用.肌浆网在肌肉兴奋-收缩耦联过程中起关键作用,与运动性骨骼肌疲劳的发生密切关.目的:通过建立SD大鼠有氧和无氧训练模型,观察不同训练负荷条件对大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶活性的影响.方法:参照Bedford TG标准,建立有氧和无氧运动大鼠跑台训练模型,有氧运动组采用递增负荷训练,无氧运动组采用高速间歇训练,正常对照组大鼠正常笼内生活,不运动.各组动物训练结束后用超速离心法提取大鼠骨骼肌肌浆网,紫外分光光度汁检测大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶的活性.结果与结论:训练4周后,两个运动组大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶的活性逐渐升高(P<0.05);训练6周,仅有氧运动组升高(P<0.05),无氧运动组则活性降低(P<0.05).结果提示有氧训练更有利十保护大鼠骨骼肌肌浆网Na+,K+-ATP酶和Ca2+-ATP酶的活性,但需要一定的时间累积.     

有氧运动对大鼠骨骼肌线粒体Na^＋,K^＋-ATP酶和Ca^2＋-ATP酶及线粒体肿胀的影响

背景：研究表明有氧运动可提高线粒体功能,但在不同时期的作用特点还不明确。目的：观察不同周期有氧运动对大鼠骨骼肌线粒体Na^＋,K^＋-ATP酶和Ca2^＋-ATP酶以及线粒体肿胀的影响。方法：将SD大鼠随机分为正常对照组,有氧运动2,4和6周组。正常对照组不进行有氧运动,其余3组则参照BedfordTG标准,采用跑台运动方式,建立有氧运动模型进行相应的运动周期锻炼。测定各组大鼠骨骼肌线粒体Na^＋,K^＋-ATP酶和Ca2^＋-ATP酶的活性以及线粒体肿胀程度。结果与结论：有氧运动2周组各指标与对照组比较无差异。有氧运动4和6周组线粒体Na^＋,K^＋-ATP酶、Ca2^＋-ATP酶活性均增高（P〈0.05）,线粒体肿胀程度降低（P〈0.05）。实验结果表明,有氧运动可保护线粒体Na^＋,K^＋-ATP酶、Ca2^＋-ATP酶的活性,提高线粒体功能,但需要一定的时间积累。     

线粒体酶活性及线粒体肿胀与不同运动强度的关系

背景：关于不同运动强度对机体的影响早有研究,并且取得了不少有价值的成果。但是对于不同运动强度对线粒体Na＋,K＋-ATP酶、Ca2＋-ATP酶活性以及线粒体肿胀程度影响的研究较少。目的：观察不同运动强度对大鼠骨骼肌线粒体Na＋,K＋-ATP酶和Ca2＋-ATP酶以及线粒体肿胀的影响。方法：将24只SD大鼠随机分为正常对照组,中等强度运动组和高强度运动组。正常对照组大鼠正常笼内生活,不运动。另2组游泳训练方式,分别建立中强度和高强度运动模型,进行相应的运动锻炼,训练4周。结果与结论：中强度运动组线粒体Na＋,K＋-ATP酶、Ca2＋-ATP酶活性与正常对照组相比均增高（P〈0.05）,线粒体肿胀程度降低（P〈0.05）;而高强度运动组线粒体Na＋,K＋-ATP酶、Ca2＋-ATP酶活性与正常对照组相比均降低（P〈0.05）,线粒体肿胀程度增大（P〈0.05）。实验结果表明中强度运动可以保护线粒体Na＋,K＋-ATP酶、Ca2＋-ATP酶的活性,提高线粒体功能;而高强度运动则降低了线粒体的功能。     

骨骼肌肌浆网Na^＋,K^＋-ATP酶和Ca^2＋-ATP酶活性在不同训练条件下的变化

背景：Na^＋,K^＋-ATP酶和Ca^2＋-ATP酶在物质运送、能量转换以及信息传递方面具有重要作用。肌浆网在肌肉兴奋-收缩耦联过程中起关键作用,与运动性骨骼肌疲劳的发生密切关。目的：通过建立SD大鼠有氧和无氧训练模型,观察不同训练负荷条件对大鼠骨骼肌肌浆网Na^＋,K^＋-ATP酶和Ca^2＋-ATP酶活性的影响。方法：参照BedfordTG标准,建立有氧和无氧运动大鼠跑台训练模型,有氧运动组采用递增负荷训练,无氧运动组采用高速间歇训练,正常对照组大鼠正常笼内生活,不运动。各组动物训练结束后用超速离心法提取大鼠骨骼肌肌浆网,紫外分光光度计检测大鼠骨骼肌肌浆网Na^＋,K^＋-ATP酶和Ca^2＋-ATP酶的活性。结果与结论：训练4周后,两个运动组大鼠骨骼肌肌浆网Na^＋,K^＋-ATP酶和Ca^2＋-ATP酶的活性逐渐升高（P〈0.05）;训练6周,仅有氧运动组升高（P〈0.05）,无氧运动组则活性降低（P〈0.05）。结果提示有氧训练更有利于保护大鼠骨骼肌肌浆网Na^＋,K^＋-ATP酶和Ca^2＋-ATP酶的活性,但需要一定的时间累积。     

脂氧素A4对内毒素攻击的肺泡Ⅱ型上皮细胞Na+-K+-ATP酶的影响

目的 探讨促炎症消退介质脂氧素A4(LipoxinA4,LXA4)对内毒素(endotoxin)攻击的大鼠肺泡Ⅱ型上皮细胞(Alveolar type Ⅱ epithelial cells,ATⅡ)Na+-K+-ATP酶的影响.方法 AT Ⅱ成功分离纯化后随机(随机数字法)分为5组:①空白组(PBS);②溶剂对照组(乙醇,0.7μL/mL);③脂多糖(lipopolysaccharide,LPS)(1μg/mL)组;④LXA4(1×10-7mol/mL)组;⑤LPS(1μg/mL)+LXA4(1×10-7mol/mL)组.药物干预4 h后用RT-PCR法检测ATⅡ上Na+-K+-ATP酶α1,β1亚基的mRNA的表达,用高效液相法测定细胞ATP,ADP,AMP和腺嘌呤核苷酸总量(TAN),间接测得Na+-K+-ATP酶的活性和AT Ⅱ能荷.结果 RT-PCR结果显示:LPS组α1,β1亚基的mRNA表达较空白组明显降低(P＜0.05),而LPS+LXA4组的α1,β1亚基的mRNA表达较LPS模型组有明显增高(P＜0.05).酶活性检测结果显示:LPS组Na+-K+-ATP酶活性较空白组明显增高(P＜0.05).与LPS刺激组比较,LPS+LXA4组酶活性明显增高(P＜0.05).能荷结果显示:LPS组较空白组明显增高(P＜0.05),其余各组间差异无统计学意义(P＞0.05).结论 LXA4能上调内毒素攻击的大鼠肺泡Ⅱ型上皮细胞Na+-K+-ATP酶α1,β1亚基mRNA表达,增强Na+-K+-ATP酶的活性,并能有效维持细胞的能量代谢平衡,提示LXA4可能通过上调Na+-K+-ATP酶的基因表达和功能活性,维持细胞代谢稳定,从而起到促进肺泡水肿液清除的作用.     

茶多酚对急性运动后大鼠骨骼肌组织损伤的保护作用

目的:探讨茶多酚对急性运动后大鼠骨骼肌组织损伤的保护作用。方法:30只SD大鼠分为对照组(A)、运动组(B)和运动加茶多酚组(C),建立力竭运动模型,1周后测试骨骼肌组织钙离子(Ca2+)含量、钠泵(Na+-K+-ATP酶)和钙泵(Ca2+-ATP酶)活性,以及在电镜和光镜下观察腓肠肌的形态和超微结构的变化。结果:运动组与对照组相比,骨骼肌组织Ca2+含量显著升高(P<0.05),Ca2+-ATP酶和Na+-K+-ATP酶的显著下降(P<0.05),运动加茶多酚组与运动组相比,骨骼肌Ca2+含量显著减少(P<0.05),Ca2+-ATP酶活性有上升趋势,Na+-K+-ATP酶活性显著升高(P<0.05)。光镜和电镜观察运动组有明显的形态学变化和超微结构的损伤,运动加茶多酚组的超微结构损伤有明显改善。结论:茶多酚可降低急性运动后骨骼肌组织中钙离子的含量,修复骨骼肌组织的损伤。     

后肢固定大鼠腓肠肌酶活性与银杏叶提取物EGB761的影响

目的:观察银杏叶提取物EGB761对后肢固定大鼠腓肠肌Na -K -ATP酶及Ca2 -ATP酶活性的影响,探讨其对失用性骨骼肌萎缩的防治作用。方法:实验于2005-04/2006-03在广州南方医院创伤骨科实验室(广东省重点实验室)完成。①实验分组:雄性SD大鼠24只,体质量200～260g,随机数字表法分为空白组、对照组、实验组,每组8只。②实验方法:制备大鼠骨骼肌失用性萎缩模型,将大鼠右后肢用可塑性石膏由足跖管型固定至膝上1cm处,膝关节固定于屈曲位100°,踝关节固定于跖屈60°,对照组给予蒸馏水3mL/d灌胃,实验组给予银杏叶提取物EGB761水溶液灌胃(灌胃剂量120mg/(kg·d),浓度14g/L)。③实验评估:4周后切取右后肢腓肠肌,去除腱膜、肌腱和神经,进行酶活性检测。结果:纳入大鼠24只,均进入结果分析。与空白组相比,对照组和实验组腓肠肌Na -K -ATP酶及Ca2 -ATP酶活性显著下降(P<0.05)。与对照组相比,实验组Na -K -ATP酶及Ca2 -ATP酶活性显著高于对照组(P<0.05)。结论:银杏叶提取物EGb761能够显著提高失用性萎缩骨骼肌Na -K -ATP酶及Ca2 -ATP酶活性,从而有效抑制骨骼肌失用性萎缩的发生。     

红细胞溶血液Na+-K+-ATP酶活力测定

目的建立利用红细胞溶血液测定红细胞Na+-K+-ATP酶活力测定方法.方法用蒸馏水将红细胞破坏,测其血红蛋白含量及红细胞Na+-K+-ATP酶活力,并与用红细胞膜酶测定法进行相关性比较.结果健康成人红细胞溶血液Na+-K+-ATP酶活力为4.345±1.175μmol Pi/gHb@h;两种方法的相关系数为0.685.结论利用红细胞溶血液进行红细胞Na+-K+-ATP酶活力测定具有操作简便,结果准确的特点,更适合于一般实验室开展.     

不同运动方式和时间对大鼠骨骼肌线粒体呼吸链复合体酶Ⅰ和Ⅳ活性的影响

背景:急性剧烈运动对机体可造成氧化应激,线粒体生成活性氧造成机体氧化应激和钙离子超负荷,导致骨骼肌功能下降,机体产生疲劳.然而长期规律运动后线粒体产生适应性变化,从而起到保护机体免受过多活性氧损害的作用.目的:观察不同运动方式和时间对大鼠骨骼肌线粒体呼吸链复合体酶Ⅰ,Ⅳ活性的影响.方法:48只健康雄性SD大鼠随机等分为正常对照组、无氧运动组、有氧运动组和交替运动组.在大鼠运动2,4,6周的时候分别处死,差速离心提取大鼠骨骼肌线粒体,分光光度法测定线粒体呼吸链复合体酶Ⅰ,Ⅳ的活性.结果与结论:运动后有氧组、交替组与无氧组线粒体呼吸链复合体酶I的活性随时间先增强而后下降;运动后有氧组与交替组线粒体呼吸链复合体酶Ⅳ的活性随时间而增强,无氧组则下降.说明有氧运动在中长期耐力运动中可有效提高大鼠体内呼吸链复合体酶Ⅰ,Ⅳ的活性,而无氧运动则只能在短期内提高其活性,长时间无氧运动可能导致对线粒体呼吸链复合体酶的损伤,影响骨骼肌工作效率,造成机体疲劳.     

光量子处理对血液保存中红细胞Na~+-K~+-ATP酶和Ca~(2+)-Mg~(2+)-ATP酶活性的影响

红细胞膜上具有Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶,其对红细胞内外离子浓度的稳定,维持细胞正常形态具有重要作用[1].维持和提高这两种酶的活性有利于血液体外保存.为此,笔者观察了全血经光量子处理前后并保存21d期间两种酶的活性变化,以探讨光量子处理血液对红细胞膜Na+-K+-ATP酶和Ca2+-Mg2+-ATP酶活性的影响.     

内毒素休克大鼠肝线粒体H+-ATP酶活性变化的研究

目的：研究内毒素休克时线粒体呼吸功能的变化及其与 Ｈ＋ Ａ Ｔ Ｐ酶活性变化的关系。方法：测定内毒素休克大鼠肝线粒体呼吸控制率（ Ｒ Ｃ Ｒ）、磷氧比（ Ｐ／ Ｏ）和 Ｈ＋ Ａ Ｔ Ｐ酶活性的变化;并通过体外孵育实验研究离体情况下不同浓度梯度细菌内毒素（ Ｌ Ｐ Ｓ）对线粒体 Ｒ Ｃ Ｒ、 Ｐ／ Ｏ 和 Ｈ＋ Ａ Ｔ Ｐ酶活性的影响。结果：内毒素休克早期,大鼠肝线粒体 Ｒ Ｃ Ｒ、 Ｐ／ Ｏ 及 Ｈ＋ Ａ Ｔ Ｐ酶活性显著增强,晚期则显著减弱。而 Ｌ Ｐ Ｓ与线粒体共同孵育导致线粒体 Ｒ Ｃ Ｒ、 Ｐ／ Ｏ 和 Ｈ＋ Ａ Ｔ Ｐ酶活性下降。线粒体 Ｈ＋ Ａ Ｔ Ｐ酶活性的变化和 Ｒ Ｃ Ｒ、 Ｐ／ Ｏ 的变化有较好的一致性。结论： Ｈ＋ Ａ Ｔ Ｐ酶活性的变化可能是内毒素休克线粒体功能变化的重要原因之一;提出了内毒素休克时线粒体功能早期增强晚期减弱的观点。     

H+-ATPase activity in selective disruption of H+-K+-ATPase alpha 1 gene of mice under normal and K-depleted conditions

The outer medullary collecting duct (OMCD) plays an important role in acid-base homeostasis by two luminal proton ATPases, H(+)-ATPase and H(+)-K(+)-ATPase (HKA), both of which are in the intercalated cells (ICs) of OMCD. We showed previously that HKAalpha1 (gastric H(+)-K(+)-ATPase) activity is the essential H(+)-K(+)-ATPase activity under normal conditions, and that HKAalpha2 (colonic H(+)-K(+)-ATPase) is induced and mediates increased proton-secretion under K-depleted conditions. To better understand the role of H(+)-ATPase (potassium-independent) in acid secretion and the relationship between H(+)-ATPase and a specific HKA isoform, we examined H(+)-ATPase activity in the H(+)-K(+)-ATPasealpha1 knockout (KO) mice under normal and K-depleted conditions. Mice were fed a potassium-free diet and studied after 7 days. Segments of the OMCD were perfused in vitro, and intracellular pH (pH(i)) was measured by ratiometric fluorescence microscopy using the pH-sensitive indicator BCECF-AM. The isolated OMCD tubules obtained from mice fed a potassium-free diet were examined by fluorescent immunocytochemistry with an antibody to the 31-kDa subunit of H(+)-ATPase (E-11) and were compared with those obtained from a normal diet. In the absence of Na(+) and K(+), the H(+)-ATPase-mediate pH(i) recovery rates were 6.7 +/- 1.1 x 10(-4) units/s (n = 7 ICs) in wild-type (WT) mice and increased to 8.7 +/- 1.8 x 10(-4) (P < 0.05; n = 6) in HKAalpha1 KO mice. K-independent proton transport activity was significantly inhibited by the H(+)-ATPase inhibitor bafilomycin A(1) (BAF, 10 nM) with luminal applied in both WT and KO mice. Comparison of the results indicated upregulation of BAF-sensitive H(+)-ATPase activity in KO mice. To determine the intracellular localization of H(+)-ATPase in the intercalated cells of OMCD, we dissected the OMCD and performed fluorescent immunocytochemistry with the H(+)-ATPase antibody in the WT and KO mice. In the WT mice, on normal diet, H(+)-ATPase staining distributed diffusely throughout the intercalated cells and was slightly polarized to the apical plasma membrane in the KO mice, consistent with increase in the H(+)-ATPase-mediate pH(i) recovery in the KO mice. One week of a potassium-free diet resulted in a significant increase in the degree of H(+)-ATPase polarization at the apical plasma membrane in both WT and KO mice. Hypokalemia stimulates H(+)-ATPase in the intercalated cells of OMCD of both WT and KO mice. The enhanced activity of H(+)-ATPase plays an important role in compensatory proton secretion in the HKAalpha1 KO mice under normal conditions.     

maFGF对慢性衰老大鼠肝组织中ATP酶活力的影响

目的观察改构型酸性成纤维细胞生长因子(maFGF)对D-半乳糖致衰老大鼠肝组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力的影响,探讨maFGF抗衰老的机制。方法选择成年Wistar大鼠40只,采用皮下注射D-半乳糖建立衰老模型,衰老模型成功后随机分为衰老对照组、NS对照组和maFGF治疗组各10只。另10只不注射D-半乳糖作为正常对照组。maFGF治疗组按12μg/kg剂量肌肉注射ma FGF,1次/d,共14 d,NS对照组肌肉注射与maFGF治疗组相同容量的生理盐水,1次/d;衰老对照组不作任何干预。各组大鼠到相对应的时间点取出各组大鼠肝组织,测定肝组织匀浆中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力。结果与正常对照组相比,衰老对照组大鼠肝组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力均明显降低(P<0.01);maFGF治疗组肝组织中Na+-K+-ATP酶活力和Ca2+-Mg2+-ATP酶活力均明显高于衰老对照组、NS对照组(P<0.05)。结论 maFGF能升高衰老大鼠肝组织中Na+-K+-ATP酶活力及Ca2+-Mg2+-ATP酶活力,对衰老大鼠肝损伤有一定保护作用。     

Increased intracellular calcium and decreased activities of leucocyte Na+,K+-ATPase and Ca2+-ATPase in asthma.

The present study was carried out to determine the intracellular free calcium concentration ([Ca(2+)](i)) and the activity of its regulatory enzymes (Na(+),K(+)-ATPase and Ca(2+)-ATPase) in leucocytes. Levels of plasma lysophosphatidylcholine (LPC) were also measured. Then the relationship between these parameters and the clinical severity of asthma and bronchial reactivity was studied. Patients with asthma were divided into three groups: acute asthma (subjects in acute exacerbation), uncontrolled asthma (subjects currently symptomatic) and stable asthma (subjects currently asymptomatic). A group of normal subjects was also studied. Spirometry, specific airway conductance and bronchial reactivity measurements were carried out. The following biochemical parameters were studied in venous blood: leucocyte [Ca(2+)](i), Na(+), K(+)-ATPase and Ca(2+)-ATPase activities, and plasma LPC. Leucocyte [Ca(2+)](i) was increased and the activities of Na(+),K(+)-ATPase and Ca(2+)-ATPase were decreased in patients with asthma. Plasma levels of LPC were also increased. These changes were observed to be greatest among asthmatics in acute exacerbation of asthma, and lesser in magnitude in patients with less severe asthma. The activities of both ATPases were found to have a significant positive correlation, and [Ca(2+)](i) and the levels of plasma LPC a significant negative correlation, with predicted forced expiratory volume in 1 s (FEV(1)). No significant correlation was observed between the biochemical parameters and bronchial reactivity. It is concluded that intracellular calcium homoeostasis is abnormal in asthma; specifically, the activities of Na(+),K(+)-ATPase and Ca(2+)-ATPase are decreased. These abnormalities may modulate the clinical severity of asthma.     

次声作用后大鼠心肌细胞内钙离子变化与L型钙通道、Ca2＋-ATP酶及Na＋-K＋-ATP酶变化的关系

目的：观察不同时间次声作用后大鼠心肌细胞钙离子变化与L型钙通道、Ca^2＋-ATP酶及Na^＋-K^＋-ATP酶变化的关系. 方法：实验于2005-04/2006-08在解放军第四军医大学西京医院次声实验室完成.①实验分组：选择健康雄性SD大鼠32只,按随机数字表法分为4组,每组8只.次声暴露1,7,14 d组（大鼠置于5 Hz/130 dB次声舱中,次声作用2 h/次,1次/d）,正常对照组（不予次声暴露）.②实验评估：测定大鼠心肌细胞内钙离子荧光强度,作为反映钙离子浓度的指标;测定L型钙通道mRNA的表达;测定Ca^2＋-ATP酶及Na^＋-K^＋-ATP酶活性. 结果：①随着次声作用时间延长,大鼠心肌细胞钙离子浓度和L型钙通道mRNA的表达明显高于正常对照组（P＜0.01）.②次声暴露1 d组大鼠心肌细胞Ca^2＋-ATP酶及Na^＋-K^＋-ATP酶的活性显著高于正常对照组（P＜0.01）,次声暴露7 d与14 d组大鼠心肌细胞Ca^2＋-ATP酶及Na^＋-K^＋-ATP酶的活性显著低于正常对照组（P＜0.01）. 结论：5 Hz/130 dB次声引起大鼠心肌钙离子浓度的时间依赖性变化,这种变化可能与L型钙通道、Ca^2＋-ATP酶及Na^＋-K^＋-ATP酶的活性变化有关.     

山莨菪碱对兔海水淹溺型肺水肿组织钠-钾-ATP酶活性的影响

目的 观察山莨菪碱(654-2)对兔海水淹溺型肺水肿组织Na -K -ATP酶活性的影响,探讨654-2对海水淹溺型肺水肿的防治作用及可能机制.方法 将35只新西兰兔随机分为对照组(5只)、淹溺组(15只)和治疗组(15只).淹溺组和治疗组根据观察时间段分为30、60、120 min组(每组5只),淹溺组采用气管切开插入塑料导管、向气管内灌海水3 mL/kg、双肺自主通气的方法进行兔海水淹溺型肺水肿模型复制;治疗组在上述基础上加用654-2静脉注射.于各观察时间点采集肺组织标本,对肺组织匀浆Na -K -ATP酶进行测定.结果 兔海水淹溺型肺水肿各时间点Na -K -ATP酶活性降低,动脉血气显示低氧和酸中毒,治疗组各时间点Na -K -ATP酶活性不同程度上升,缺氧和酸中毒改善(P<0.05).结论 654-2对兔海水淹溺型肺水肿的减轻作用可能与其能够上调肺组织Na -K -ATP酶活性有关.     

颈椎椎后肌肉组织中肌膜Na^＋-K^＋-ATP酶活性与颈椎病

目的:探讨颈椎椎后肌肉组织Na -K -ATP酶活性变化与颈椎病的关系。资料来源:应用计算机检索PubMed1988-01/2004-12相关骨骼肌损伤与肌组织Na -K -ATP酶关系的文献,检索词“Na -K pump,Na -K -ATPase,muscle”,限定文献语言种类为English。同时计算机检索CNKI1990-01/2005-12相关Na -K -ATP酶与骨骼肌损伤的关系及颈椎病发病病因的文献,检索词“Na -K -ATP酶,骨骼肌,颈椎病病因”,限定文献语言种类为中文。资料选择:对资料进行初审,选取包括Na -K -ATP酶与肌组织损伤关系的文献,开始查找全文。纳入标准:Na -K -ATP酶活性变化与骨骼肌损伤密切相关的文献研究。排除标准:重复研究,Meta分析类文章。资料提炼:共检索到939篇关于Na -K -ATP酶与骨骼肌损伤相关方面的文献,最终纳入20篇符合标准的文献。资料综合:众多研究表明,Na 、K 与骨骼肌的兴奋、收缩、疲劳有密切关系,而Na -K -ATP酶又是调节细胞内外Na 、K 浓度必不可少的高分子蛋白,也就是说,骨骼肌一系列活动均离不开Na -K -ATP酶,Na -K -ATP酶活性变化与骨骼肌损伤是相互影响的。而强迫屈颈体位作为颈椎病发病的危险因素之一,可使颈椎椎后肌肉Na -K -ATP酶活性降低,酶活性降低致使肌细胞损伤,并最终导致骨骼肌损伤而发病。结论:以颈椎椎后肌肉酶活性的变化来阐释中医药对颈椎病确切疗效的相关研究未见,这有待于进一步研究,以充分展示中医药在颈椎病等相关疾病中的治疗优势。     

In vivo effects of high phenylalanine blood levels on Na+,K+-ATPase,Mg2+-ATPase activities and biogenic amine concentrations in phenylketonuria

OBJECTIVE: To evaluate the activities of Na+,K+-ATPase and Mg2+-ATPase in erythrocyte membranes from phenylketonuric (PKU) patients and to correlate the enzyme activities with their blood phenylalanine (Phe) levels, biogenic amines as well as with their precursors tyrosine (Tyr) and tryptophan (Try). DESIGN AND METHODS: Twenty three PKU patients were divided into group A (n = 12) on a restricted diet (Phe 1.57 +/- 0.52 mg/dL or 0.10 +/- 0.03 mM) and group B (n = 11) on a "loose" diet (Phe 24.45 +/- 1.50 mg/dL or 1.72 +/- 0.09 mM). The enzyme activities were measured spectrophotometrically, the amino acids with an automatic amino analyser and the biogenic amines with HPLC methods. RESULTS: In group B, plasma amino acids (Tyr, Try), their biogenic amines [adrenaline (A), noradrenaline (NA), dopamine (DA) and serotonin (5HT)], (Na+,K+)-ATPase and Mg2+-ATPase activities were found remarkably decreased (p < 0.001). CONCLUSIONS: High Phe and/or low NA, DA, 5HT plasma levels may indirectly inhibit the erythrocyte membrane Na+,K+-ATPase and Mg2+-ATPase in PKU patients. The observed enzyme inhibitions could be a very informative peripheral marker as regards the neurotoxic Phe brain effects.     

针刺手厥阴心包经穴对缺血/再灌注大鼠心肌离子泵的影响

目的:观察针刺心包经穴对大鼠心肌缺血/再灌注损伤过程中心肌细胞Na -K -ATP酶和Ca2 -Mg2 -ATP酶活性的影响,探讨其心肌保护作用的机制.方法:50只大鼠随机分为5组.假手术组只穿线不结扎冠状动脉,其余各组制备缺血/再灌注动物模型,其中3个针刺穴位组分别于电针大鼠内关穴、郄门穴或支沟穴20 min后,结扎冠状动脉左前降支40 min,心电图监测,再电针相应穴位20 min,恢复灌流.假手术组于穿线后100 min、模型组和各针刺穴位组于再灌注60 min摘取心脏,取心室肌制备心肌细胞膜,定磷法观察Na -K -ATP酶和 Ca2 -Mg2 -ATP酶活性的变化.结果:针刺心包经穴(内关、郄门)组Na -K -ATP酶和 Ca2 -Mg2 -ATP酶活性均明显升高,与模型组比较差异均非常显著(P均<0.01).结论:针刺手厥阴心包经穴可提高Na -K -ATP酶和Ca2 -Mg2 -ATP酶活性,减轻心肌细胞钙超载程度,有效地保护心肌.