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1.
研究正常青年人(青年对照组)、与患者同龄之正常人(同龄对照组)及冠心病患者红细胞膜Na~+-K~+ATP酶、Ca~(2+)ATP酶和Mg~(2+)ATP酶的活性;观察了运动试验和钙拮抗剂硝苯吡啶对上述三种酶活性的影响。结果表明:同龄对照组的三种ATP酶活性均低于青年对照组;静息状态下,冠心病患者的Na~+-K~+ATP酶活性低于同龄对照组,而Mg~(2+)ATP酶活性高于同龄对照组;运动试验后,同龄对照组Na~+-K~+ATP酶、冠心病组Na~+-K~+ATP酶和Ca~(2+)ATP酶活性增高。冠心病患者服用硝苯吡啶后,前述的ATP酶的改变不复存在。  相似文献   

2.
测定20例正常人及40例 NIDDM 患者红细胞膜 ATP 酶活力和红细胞内离子浓度。结果NIDDM 患者 Na~+-K~+-ATP 酶、Ca~(2+)-ATP 酶活力明显低于正常人(P 均<0.001),Mg~(2+)-ATT 酶活力无明显改变(P>0.05);NIDDM 患者红细胞内[Na~+]、[Ca~(2+)]明显高于正常人(P 分别<0.001和0.01),[Mg~(2+)]明显低于正常人(P<0.001),[K~+]无明显变化(P>0.05)。上述变化在无血管病者就已出现,有血管病者更加明显。  相似文献   

3.
本文初步观察了正常人中分子物质(N-MMS)和烧伤病人中分子物质(B-MMS)对正常人红细胞膜Ca~(2+)-ATP酶活力的影响。结果表明,不同保温时间N-MMS对红细胞膜Ca~(2+)-ATP酶活力有明显影响,保温时间越长酶活力抑制越显著(p<0.01),对照组变化不明显;不同浓度N-MMS和B-MMS对红细胞膜Ca~(2+)-ATP酶活力均有影响,浓度越高酶活力抑制越明显(P<0.01)。MMS对质膜Ca~(2+)-ATP酶的抑制作用可能是MMS导致细胞病理变化的一个重要环节。  相似文献   

4.
目前对钙-钙调素(Calmoclulin,CaM)与遗传性高血压发病的关系报道很多。在对自发性高血压大鼠(SHR)的研究中,已证实钙代谢障碍主要表现在细胞内钙浓度及钙与膜的结合、转运、与CaM的结合和囊泡摄取等多环节的异常。由于红细胞膜具有除Na~+-Ca~(2+)交换以外的各种主动及被动的阳离子转运系统及99%的可交换钙都容纳在单一库内的双重优点,加之其取材方便,制备简单,因而我们对钙通道阻断剂心痛定治疗前后SHR红细胞膜Ca~(2+)-Mg~(2+)ATP酶,Mg~(2+)ATP酶活性进行了研究。  相似文献   

5.
对10例Duchenne型肌营养不良(DMD)患者红细胞膜进行了膜糖、脂质及Ca~(2+)-Mg~(2+)ATP酶活力的研究。结果为DMD红细胞膜唾液酸显著减少,而中性糖含量无变化;膜磷脂含量无明显改变,但膜胆固醇显著增加,磷脂/胆固醇之比显著降低,膜Ca~(2+)-Mg~(2+)ATP酶活力显著升高。表明DMD红细胞膜有组成和功能上的改变。  相似文献   

6.
细胞膜上的ATP和Mg~(2 )依赖性的Ca~(2 ),Mg~(2 )-ATP酶(即钙泵)的基本功能是主动转运Ca~(2 ),维持胞内Ca~(2 )的相对恒定.细胞内Ca~(2 )浓度持续升高将会危及细胞的各种功能.细胞膜Ca~(2 )转运障碍与高血压发病有密切关系.红细胞膜是研究各种浆膜Ca~(2 )转运的理想模型.作者改进了文献方法.建立了以红细胞膜IOV来研究Ca~(2 )摄取的方法,为研究高血压发病过程中细胞膜Ca~(2 )的摄取异常机理,提供了一种可靠的手段.  相似文献   

7.
原发性高血压钙恒稳异常不仅表现在血管平滑肌,也见于其它组织细胞,尤其是血液的有形成分。本文观察了原发性高血压患者红细胞的某些钙恒稳指标,并与正常人进行了比较。结果表明:高血压患者红细胞总钙浓度较正常人明显增加,红细胞膜Ca~(2+)-ATP酶活性明显降低,胞浆钙调素含量显著降低。结果提示:高血压患者红细胞Ca~(2+)-ATP酶活性下降导致胞内Ca~(2+)浓度升高,从而增加外周血管阻力,而CaM可能是通过调节Ca~(2+)-ATP酶活性间接影响血压的。  相似文献   

8.
本文采用Murphy的超速离心法,将10名我国正常人的红细胞分为三个龄组,以HPLC和酶学方法测定不同龄红细胞的几种核苷酸含量及膜ATP酶活性。结果表明,正常人红细胞内ATP含量和NAD含量随细胞老化而降低,但ADP、AMP,和NADP含量的改变不明显;红细胞膜的Mg~(2+)—ATP酶和Ca~(2+)—ATP酶活性亦随红细胞老化而降低,其Na~+,K~+—ATP酶活性的改变不明显。  相似文献   

9.
目的:观察脾阴虚证大鼠回肠组织中Na+-K+ATP酶、Ca~(2+)-Mg~(2+)ATP酶及线粒体呼吸链酶复合物Ⅰ、Ⅳ活性在理脾阴正方干预下发生的变化,分析理脾阴正方通过滋养脾胃、舒展脾气之法以改善脾阴虚证的作用机理,探讨其对能量代谢可能产生的影响。方法:采取饮食不节结合劳倦过度之法建立脾气虚大鼠模型,在此基础上运用辛热伤阴法复制脾阴虚大鼠模型,对健康对照组、脾阴虚模型组、脾阴虚中药反证组用比色法检测大鼠回肠组织中Na+-K+ATP酶、Ca~(2+)-Mg~(2+)ATP酶及线粒体呼吸链酶复合物Ⅰ、Ⅳ活性。结果:(1)脾阴虚模型组回肠组织Na+-K+ATP酶、Ca~(2+)-Mg~(2+)ATP酶及线粒体呼吸链酶复合物Ⅰ、Ⅳ活性均显著低于健康对照组(P0.05),结果有统计意义。(2)脾阴虚中药反证组回肠组织Na+-K+ATP酶、Ca~(2+)-Mg~(2+)ATP酶及线粒体呼吸链酶复合物Ⅰ、Ⅳ活性明显高于脾阴虚模型组(P0.05),结果有统计意义。结论:理脾阴正方能够提高脾阴虚模型大鼠回肠组织中Na+-K+ATP酶、Ca~(2+)-Mg~(2+)ATP酶及线粒体呼吸链酶复合物Ⅰ、Ⅳ活性,纠正脾阴虚证,其作用可能与细胞能量代谢有关。  相似文献   

10.
以被动吸烟致胎儿宫内发育延缓(IUGR)大鼠为模型,观察了活血化瘀方对孕鼠红细胞膜Ca~(2+)-ATP酶活性的影响。结果表明:模型组胎仔出生平均体重、Ca~(2+)-ATP酶活力均低于对照组(P<0.01),用药组与对照组之间差异无显著意义(P>0.05),且胎仔平均出生体重与Ca~(2+)-ATP酶活性呈正相关关系(r=0.3446,P<O.05)。从而提示本方能提高Ca~(2+)-ATP酶活性,保护红细胞正常形态与功能,从而改善胎盘血液循环,促进胎儿发育。  相似文献   

11.
OBJECTIVE: To assess the relationships between plasma and intracellular Ca2+, Mg2+ and blood cell membrane adenosine triphosphatase (ATPase) activity in normotensive and hypertensive subjects. METHODS: Plasma and intracellular Ca2+, Mg2+ were measured with atomic absorption spectrophotometry, and red blood cell membrane Na(+)-K+ ATPase and Ca(2+)-ATPase activities were determined with colorimetric method in 55 patients with essential hypertension and 32 normotensive controls. RESULTS: The results showed that the hypertensive group consistently demonstrated a significant decreased activity of ATPase studied, with significantly lower plasma Ca2+ and higher cytosolic Ca2+ levels when compared with those in normotensive group (P < 0.01 or P < 0.05, respectively). No significant differences were found in either plasma Mg2+ or intracellular Mg2+ level between the two groups. CONCLUSIONS: This study suggests that patients with essential hypertension have widespread depression of cell membrane Na(+)-K(+)-ATPase and Ca(2+)-ATPase activities with plasma Ca2+ depletion and cytosolic Ca2+ overload, which may reflect an underlying membrane abnormality in essential hypertension. The cellular abnormalities may be related to the defective transport mechanisms that in turn may be aggravated by plasma Ca2+ depletion.  相似文献   

12.
Summary The effect of Huoxuequyu recipe on erythrocyte membrane Ca2+-ATPase activity in pregnant rats with passive smoking induced asymmetrical intrauterine growth retardation (IUGR) was observed. The rats were divided into three groups: control group, model group and treated group. The fetal mean birth weight and erythrocyte membrane Ca2+-ATPase activity were found to be decreased in the model group as compared with the control and treated groups. There was a significant difference between the model group and the control group (P<0.01), while no significant difference existed between the treated group and the control group (P>0. 05). Furthermore, the findings indicated that the erythrocyte membrane Ca2+-ATPase activity seem to be positively correlated with the birth weight (P<0. 05). On the basis of our observation, it is believedthat the Huoxuequyu decoction could increase erythrocyte membrane Ca2+-ATPase activity and promote blood circulation, thereby exerting a beneficial effect on fetal development. This project is supported by the National Natural Sciences Foundation of China. No 39270826  相似文献   

13.
用酶解法和H2O2分解法分别测定28例风心瓣膜病变患者红细胞膜钠泵(Na+、K+-ATP酶)、钙泵(Ca2+、Mg2+-ATP酶)活性和膜过氧化氢酶(CAT)活性,并用硫代巴比妥酸比色法测定患者红细胞膜脂质过氧化物(LPO)含量。患者红细胞膜Na+、K+-ATP酶活性和Ca2+、Mg2+-ATP酶活性分别显著低于正常人34.75%(P<0.01)和26.77%(P<0.01);CAT活性显著低于正常人20.07%(P<0.01);而患者LPO含量却显著高于正常人97.50%(P<0.01)。结果提示风心病患者瓣膜病变与质膜钠、钙泵活性变化以及膜脂质过氧化作用有关。  相似文献   

14.
Background  Abnormal insulin secretion of pancreatic beta cells is now regarded as the more primary defect than the insulin function in the etiology of type 2 diabetes. Previous studies found impaired mitochondrial function and impaired Ca2+ influx in beta cells in diabetic patients and animal models, suggesting a role for these processes in proper insulin secretion. The aim of this study was to investigate the detailed relationship of mitochondrial function, Ca2+ influx, and defective insulin secretion.
Methods  We investigated mitochondrial function and morphology in pancreatic beta cell of diabetic KK-Ay mice and C57BL/6J mice. Two types of Ca2+ channel activities, L-type and store-operated Ca2+ (SOC), were evaluated using whole-cell patch-clamp recording. The glucose induced Ca2+ influx was measured by a non-invasive micro-test technique (NMT).
Results  Mitochondria in KK-Ay mice pancreatic beta cells were swollen with disordered cristae, and mitochondrial function decreased compared with C57BL/6J mice. Ca2+ channel activity was increased and glucose induced Ca2+ influx was impaired, but could be recovered by genipin.
Conclusion  Defective mitochondrial function in diabetic mice pancreatic beta cells is a key cause of abnormal insulin secretion by altering Ca2+ influx, but not via Ca2+ channel activity.
  相似文献   

15.
ObjectiveTo study the effect of phospholamban antisense RNA (asPLB) on sarcoplasmic reticulum Ca2+-ATPase activity and cardiac function in rats with diabetes mellitus (DM) mediated by recombinant adeno-associated virus (rAAV) vector.MethodsSix weeks after the induction of DM by streptozotocin injected intraperitoneally, the rats were divided into three groups, namely: DM-rAAV-asPLB group, DM-saline group and DM group (control group). The rats in the DM-rAAV-asPLB group were intramyocardially injected with rAAV-asPLB, the rats in the DM-saline group were injected with saline, and those in the control group did not receive any treatment. Six weeks after gene transfer, the expressions of PLB protein and PLB phosphorylation were detected by Western-blot, while the activity of sarcoplasmic reticulum (SR) Ca2+-ATPase and left ventricular function were measured.ResultsThe PLB protein expression level was significantly higher whereas the PLB phosphorylation, SR Ca2+-ATPase activity and left ventricular function were significantly lower in the DM-saline group than in the control group. No significant difference was found in PLB protein expression level, PLB phosphorylation or SR Ca2+-ATPase activity between the DM-rAAV-asPLB group and the control group. The left ventricular function in the DM-rAAV-asPLB group was poorer than in the control group and was better than in the DM-saline group.ConclusionrAAV-asPLB can down-regulate PLB protein expression and up-regulate PLB phosphorylation and SR Ca2+-ATPase activity, thus contributing to the improvement of in vivo left ventricular function.  相似文献   

16.
慢性肾衰患者红细胞膜ATP酶活性及离子浓度的变化   总被引:3,自引:0,他引:3  
  相似文献   

17.
采用德国BrainScanX-刀治疗脑转移治病人43例.经过6~12个月的随访,结果表明,X-刀治疗脑转移瘤的效果理想,肿瘤生长局部控制率达95.34%,81.40%肿瘤于3~6个月内消失或明显缩小,6个月以上生存率达77.14%,无明显并发症.总结了适应症的选择,影像学要求,治疗计划的设计和优化,疗效判断标准以及并发症的防治等方面的经验和体会.  相似文献   

18.
Cardiopulmonary bypass ( CPB) can cause ery-throcytes damage.The damaged erythrocytes notonly result in hemotocytolysis and also obstruct mi-crocirculation. Recently some studies demonstratedthat Ca2 is a major factor to maintain erythrocytemembrane homeostasis and normal deformity[1] .Propofol is a rapid acting intravenous anesthetic,which possesses the properties to scavenge free radi-cals and block Ca2 channels.While whether propo-fol is effective or not in protecting erythrocytes fro…  相似文献   

19.
目的 测定妊高征患者胎盘滋养细胞线粒体ATP酶活性及氧自由基的变化,探讨其在妊高征发病机制中的作用。方法 选取妊高征患者(53例)及正常妊娠妇女(32例)胎盘,匀浆后提取线粒体。分别测定线粒体Ca^2+-Mg^2+-ATP酶、SOD的活性及MDA含量变化。结果 重度妊高征患者胎盘滋养细胞线粒体Ca^2+-Mg^2+-ATP酶、SOD活性与正常孕足月胎盘相比明显降低,而MDA含量却明显升高(P〈0.05);Ca^2+-Mg^2+-ATP酶活性与MDA含量呈负相关,而与SOD呈正相关。结论 重度妊高征患者胎盘滋养细胞线粒体ATP酶活性显著降低,自由基增多,提示自由基抑制ATP酶活性。促进妊高征病情进展。  相似文献   

20.
[目的]探讨水飞蓟宾(SIL)对Langendorff灌流大鼠离体心脏缺血再灌注损伤的保护作用及其作用机制。[方法]100只SD大鼠随机分为正常对照组、模型组、SIL低[100 mg/(kg·d)]、中[200 mg/(kg·d)]、高[400 mg/(kg·d)]剂量组,各20只;手术前2h灌胃给药,采用Langendorff灌流系统制备大鼠离体心脏灌注模型,模型组与SIL各组灌注K-H液20 min后停灌30 min、然后再灌注60 min后行各指标检测,而正常对照组持续灌注K-H液。测定冠脉流出液心肌酶活性;通过四氮唑(TTC)染色计算心脏组织梗死面积,采用苏木精-伊红(HE)染色对心脏组织进行病理学检查;测定血流动力学指标;测定抗氧化酶活性和丙二醛(MDA)含量;测定心肌组织Na+-ATPase、Ca2+-ATPase酶活力。[结果]与模型组比较,SIL中、高剂量组心肌酶:谷草转氨酶(AST)、乳酸脱氢酶(LDH)、肌酸激酶MB同工酶(CK-MB)活性显著降低,梗死面积显著降低;病理学检查结果显示:经SIL干预能够明显改善心脏组织病变;血流动力学指标明显改善[心率(HR)、左室收缩压(LVSP)、左室收缩压最大上升速率(+dP/dtmax)、左室舒张压最大下降速率(-dP/dtmin)显著升高,左室舒张压(LVEDP)显著降低];抗氧化酶:超氧化物歧化酶(SOD)、过氧化氢酶(CAT)活性显著升高且MDA含量显著降低;Na+-ATPase、Ca2+-ATPase酶活力显著升高,上述结果差异具有统计学意义(P<0.05或P<0.01)。[结论]SIL对离体心脏缺血再灌注损伤具有一定的抑制作用,其作用机制可能与SIL能够改善血液流变学指标、抑制氧化应激、提高ATP酶活力有关。  相似文献   

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