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1.
实验动态观察了大鼠心肌梗塞(MI)后左、右心室及血浆中血管紧张素Ⅰ、Ⅱ(AngⅠ、Ⅱ)含量和血浆肾素活性的变化。结果表明:术后第3、15和42d,梗塞鼠左、右心室Ang Ⅰ、Ang Ⅱ的含量均显著高于假手术鼠,而血浆肾素活性及Ang Ⅰ含量与假手术组无明显差异。第3d时血浆Ang Ⅱ水平虽有明显升高,但于15d已降到对照水平。提示MI后心脏局部RAS激活,心肌中Ang Ⅰ、Ⅱ的变化与循环RAS无依存关系。  相似文献   

2.
围绕着“一种新的激素———内源性哇巴因(endogenous ouabain,EO)”,从“生物学特性和生理学研究”、“病理生理学和临床意义研究”、“检测方法”及“应用研究”四个方向展开对内源性哇巴因历时17年的系列研究,结果显示:EO是一种新的肾上腺皮质激素;EO的异常分泌与高血压等疾病的发生发展密切相关;对高EO的病理生理学作用的干预,有可能成为新的诊断和治疗方法。  相似文献   

3.
Hantaanvirus,theetiologicagentofhemorrhagicfeverwithrenalsyndrome(HFRS),canleadtoaseveretypeofHFRSandbelongstothegenusHantavirusofthefamilyBunyaviridae.ThegenomeofHantannvirusconsistsofthreesegmentsL,MandSrespectivelyencodingpolymerase,membraneglycoproteinG,andG,andnucleoproteinofthevirus.Inthepresentpaper,serumantibodiestonecleoprotein(NPAb)andglycoproteinG,(G,Ab)ofHantaanvirusinpatientswithHFRSweredynamicallydeterminedusingantibodyblockingenzymelinkedimmunosorbentassays(B--ELISA…  相似文献   

4.
探讨正常 SD大鼠血清及组织内源性哇巴因 ( EO)的含量 ,为 EO生理及病理作用的进一步研究提供理论及实验依据。方法 制备高度特异性的哇巴因抗体 ,应用酶联免疫吸附试验 ( ELISA)的方法 ,对正常 SD大鼠血清及组织标本测定其 EO含量。结果 血清、肝脏、肾脏、肾上腺、垂体及下丘脑内 EO含量分别为 ( 1 .1 2± 0 .1 7) μg/ L、( 1 .79± 0 .44) μg/ kg组织、( 1 .0 8±0 .63)μg/ kg组织、( 1 .73± 0 .81 )μg/ kg组织、( 2 7.54± 6.91 )μg/ kg组织、( 1 .83± 0 .54)μg/ kg组织、( 1 0 .1 0± 3.0 8) μg/ kg组织。肾上腺内 EO含量明显高于其它组织及血清 EO含量。结论 确定了正常 SD大鼠血清及多种组织内源性哇巴因的含量 ,提示肾上腺有可能是 EO的主要来源  相似文献   

5.
目的探讨过氧化物酶体增殖物激活受体γ(PPARγ)激动剂triglitazone对血管紧张素Ⅱ(AngⅡ)刺激内皮细胞分泌血管活性因子的影响。方法以脐静脉内皮细胞为研究对象,观察triglitazone对内皮细胞分泌血管活性因子内皮素-1(ET-1)和一氧化氮(NO)的影响。结果10μmol/L和50μmol/L的triglitazone使人脐静脉内皮细胞分泌ET-1含量与对照组相比虽有下降但无统计学意义,而NO与对照组相比明显升高(P<0.05);50μmol/L triglitazone可明显抑制AngⅡ(1×10-6mol/L)所刺激的ET的分泌(P<0.05);两种浓度triglitazone均能抑制AngⅡ对内皮细胞生成NO的减低作用(P<0.05)。结论Triglitazone可抑制AngⅡ所刺激的内皮细胞合成和分泌ET-1的增加和NO的减少,提示triglitazone可通过影响血管活性因子的产生而参与血压的调节。  相似文献   

6.
Saltsensitivityisanintermediategenotypeofessentialhypertension ,associatedwithnumerousneuro hormonalabnormalities[1,12 ] .Theregulationdysfunctionofrenin angiotensinsystemisinvolvedinsaltsensitivity ,whichconsistsoftwodifferentregulatoryresponses ,modulatorsandnon modula tors,aftersaltload[2 ,13 ] .Basedonour previousstudies ,theobjectofthisstudyistoinvestigatethechangepatternofrenin angiotensinandatrialnatri ureticpeptide(ANP)ofsaltsensitivehypertensionthroughobservingthechangesinplasmaangio…  相似文献   

7.
Objective The main purpose of this study was to investigate whether the folliculo-stellate cells (FSC) respond to angiotensin(Ang) Ⅱ by increasing intracellular free concentration ([]i) ,and where the o-rigin of mobilization is if that has occurred. Methods Pituitary cells in primary culture were prepared from male Wister rats(250g) by a conventional method and cultured in MEM supplemented with 4% normal rat serum. Af-ter 2 days in culutre,cells were loaded with 1 μmol/L fura-PE3/AM for 1 h and subjected to a ment with Quanti Cell 700 system. Excitation wavelengths of 340 and 380 nm were selected by means of a computer-controlled filterwheel. Results The of FSC in the rat anterior pituitary was elevated by Ang Ⅱ. The eleva-tion of of FSC induced by 0. 1,1.0,10 and 100 nmol/L Ang Ⅱ was (56.33±6.18), (117.07± 36.07), (175.59 ± 40.01 ) and (216.02 ±11.52) nmol/L, respectively. The increase of of FSC induced by 100nmol/L Ang Ⅱ was not influenced by the medium without (0Ca),but significantly suppressed by thapsigargin (TG),an inhibitor of ATPase. The rate of responsive FSC to Ang Ⅱ (100 nmol/L) was 61.84% which was obviously higher than that of pituitary endocrine cells (43.49%). Conclusion The present experiment demonstrates that the FSC in the rat anterior pituitary responds to Ang Ⅱ by increasing [which raises the possibility that Ang Ⅱ re-leased from either lactotrophs or gonadotrophs affects FSC through paracrine mechanism. The elevation of [induced by Ang Ⅱ presents a dosage-dependent relation, and is possibly because of the release of from an intra-cellular pool (s). Fashions of release are relative to the concentration of Ang Ⅱ. The results indicate that Ang Ⅱ functions as a paracrine factor among pituitary cells including FSC.  相似文献   

8.
目的观察PPAR-γ激活对血管紧张素Ⅱ诱导的体外培养条件下大鼠血管平滑肌(VSMCs)的细胞外基质(ECM)释放及结缔组织生长因子(CTGF)表达的影响。方法原代培养大鼠VSMCs,用不同浓度PPAR-γ激动剂rosiglitzone和/或抑制剂GW9662、BADGE预处理后,加入0.1μmol/L血管紧张素Ⅱ(AngⅡ)刺激24h。比色法检测各组细胞培养液中羟脯氨酸含量,实时荧光定量RT-PCR方法检测各组三型胶原(ColⅢ)、层粘连蛋白(FN)及CTGFmRNA表达,Western blotting检测各组CTGF、PPAR-γ蛋白表达情况,基于ELISA的DNA-binding检测各组PPAR-γ活性。结果 AngⅡ可增加VSMCs PPAR-γ表达,但明显抑制其活性(P<0.05,vs.Control),PPAR-γ激动剂rosiglitazone可显著增加PPAR-γ蛋白表达及活化(P<0.05,vs.AngⅡ)。rosiglitazone可降低细胞培养液中羟脯氨酸含量,下调VSMCs中ColⅢ、FN、CTGF mRNA表达,抑制CTGF蛋白表达,而其他PPAR-γ激动剂(pioglitazone、15-d-PGJ2)均有相似作用,PPAR-γ拮抗剂GW9662及BADGE可拮抗这一作用。结论在VSMCs中,PPAR-γ激活可抑制AngⅡ诱导的CTGF表达,同时抑制ECM沉积。提示PPAR-γ可能在血管纤维化中起重要作用。  相似文献   

9.
EXPRESSION OF ENDOGENOUS OUABAIN IN MULTIPLE ADRENAL TUMORS   总被引:1,自引:0,他引:1  
Adrenals ,whichcankeepthebalanceofinnerenvironment,areimportantendocrines ,andlotsofdiseasesarerelatedtotheirfunction .ThepresenceofanendogenousNa ,K - pumpinhibitorinmam mals ,whichcanaffectrenalNa excretion ,vascularcontractility ,andnervousreactivity ,hasb…  相似文献   

10.
螺内酯在预防大鼠肝纤维化形成中的作用   总被引:2,自引:1,他引:2  
目的 探讨螺内酯对实验性大鼠肝纤维化的预防作用及醛固酮在肝纤维化发病中的意义。方法 实验分为正常对照组、肝纤维化组、螺内酯预防组。用复合因素制备肝纤维化模型 ,螺内酯每日按 10 0mg·kg- 1 制成1mL溶液灌胃 ,观察其预防肝纤维化形成的作用。结果 ①螺内酯可使纤维化肝组织羟脯氨酸 (HYP)含量明显下降 (P <0 .0 1)。②VG染色、网状纤维染色可见螺内酯预防组肝纤维化程度明显降低 (P <0 .0 1)。③肝纤维化组血清、肝组织ALD水平较正常对照组明显升高 (P <0 .0 5 ) ;螺内酯预防组与正常对照组相比 ,血清、肝组织ALD均升高 (P <0 .0 5 )。结论 螺内酯对肝纤维化的形成有预防作用 ,醛固酮可能参与肝纤维化的形成过程  相似文献   

11.
目的 观测血管紧张素Ⅱ对体外培养的牛小梁细胞间质合成的影响 ,探讨原发性开角青光眼的发病机制。方法 ①体外培养牛眼小梁细胞 ,应用免疫组化方法 (NSE ,Ⅷ因子相关抗原染色 )鉴定细胞 ,光学及电子透射显微镜对细胞进行形态学及生长特性的观察 ;②AngⅡ (1×1 0 -7mol·L-1及 1× 1 0 -8mol·L-1)及其Ⅰ型受体拮抗剂孵育牛眼小梁细胞 ,免疫荧光染色测定纤维粘连蛋白 ,并用化学方法检测培养液中羟脯氨酸含量间接推导胶原含量。结果 牛眼小梁细胞培养成功 ,以上皮型为主。AngⅡ明显地增加了牛眼小梁细胞纤维粘连蛋白 ,同时培养液中的羟脯氨酸含量亦相应增高 (P <0 0 5 )。结论 体外培养牛眼小梁细胞技术是研究小梁细胞特性的重要实验技术。AngⅡ可以促进纤维粘连蛋白、胶原合成增强 ,AT1受体拮抗剂可以部分阻断此促增殖效应。  相似文献   

12.
目的 探讨内源性哇巴因 (Endogenous ouabain,EO)在 SD大鼠体内的组织学定位。方法 采用高度特异的抗哇巴因兔血清 ,用免疫组织化学 ABC法观察 EO在大鼠体内的分布。结果 免疫组化染色显示在 SD大鼠的肾上腺皮质内侧网状带可以观察到丰富的哇巴因免疫反应阳性物质 ,垂体后叶有较弱的哇巴因免疫反应阳性物质 ,而下丘脑、肾脏、心肌等组织中并未发现有哇巴因免疫反应阳性物质存在。结论 表明 EO主要存在于 SD大鼠肾上腺皮质网状带 ,为 EO作为一种新的肾上腺皮质激素提供了形态学依据  相似文献   

13.
目的观察慢性盐缺乏和盐负荷对内源性哇巴因(EO)分泌的影响,探讨在慢性盐缺乏或盐负荷状态下EO对SD大鼠钠代谢和血压的调节作用。方法以含0.02%(低盐)、0.5%(普食)及8%(高盐)的普通加碘盐饲料喂养SD大鼠8周,原子吸收分光光度法检测尿液中钠离子、钾离子浓度,酶联免疫吸附法(ELISA)检测EO水平。结果高盐组SD大鼠血压较同期普食组和低盐组显著性升高(P<0.01)。高盐组24 h尿钠排泄量较普食组和低盐组显著增加(P<0.01)。高盐组24 h尿钾排泄量显著低于对照组和低盐组(P<0.01)。高盐组与普食组比较血清EO水平无统计学差异,低盐组于第4周开始血清EO水平高于普食组和高盐组,有统计学差异(P<0.01)。结论慢性盐缺乏时SD大鼠EO水平升高,提示其为慢性盐缺乏状态下维持血压的调节因子;而慢性盐负荷时血压明显升高,但未发现EO显著升高。  相似文献   

14.
目的观察无肝素化体外循环期间AngⅡ、ET-1的表达水平,为临床提供参考依据。方法制备鱼精蛋白-琼脂糖凝胶柱并建立动物模型,对肝素化及无肝素化体外循环期间AngⅡ、ET-1水平进行检测。结果血浆AngⅡ及ET-1水平在组内相比,以转流开始时为对照,1、2、3h时AngⅡ及ET-1水平均逐渐升高,差异有统计学意义(P<0.05);两组间比较转流期间差异有统计学意义(P<0.05)。结论依靠鱼精蛋白-琼脂糖凝胶对凝血因子进行吸附以进行无肝素化体外循环效果明确,但通过对AngⅡ及ET-1在血浆中表达水平的评估,提示其现阶段距临床应用仍有差距。  相似文献   

15.
Autoantibodiesagainst-theadeninenecleotidetranslocator(ANT)mightplayanimportantroleinthedevelopmentofviralmyocarditis(VMC)andidiopathicdilatedcardiomyopathy(DCM)tl].ThebestwaytodescribethepathogenesisofantiANT-antibodiesistoimmuneanimalswithANT.However,difficultiesinthepreparationandstorageofnativeANTproteinsinfluencedfurtherinvestigation.Recently,accordingtotheaminoacidsequencesanddistributionofantigenicdeterminantsofANT,wesynthesizedapeptidecontaining'oneoftheantigenicdeterminantsof…  相似文献   

16.
AntigenssuchasQ-fetoproteinandcarcinoembryonicantigenhavebeenusedasmarkersforthediagnosisandpostoperativeevaluationofpatientswithmalignanttumors.Lindholmetaldetectedamalignanttumorcelllinebyusinghybridomatechniquein1983,themonoclonalantibodiessecretedbythecelllineweredefinedasC50.TheantigenrecognizedbyC50monoclonalantibodywasnamedCA50.Itwasraisedagainstacolorectaladenocarcinomacellline.CA50antigenexistsonthecellsurfaceintheformoflipidorlipoproteincomplex,belongingtothemarkerofsphingoglycoli…  相似文献   

17.
Lumbardischerniationisthemostcommoncauseoftheachingwaistsandlegs.Anaccuratediagnosisisnecessarytorighttreatment.Beforeoperation,electrophysiologicalexaminationisthebestsupplementarytoimageology.Itcanhelpustodiagnosetheradiculopathycausedbytheoccupativediseasesorthenon--occupativediseases.andtoevaluatetheprognosis.Magneticstimulation,asanon-invasiveelectrophysiologictechniquehasbeenusedintheclinicaldiagnosisoflumbardischerniationtl~4).Yetuptonow,therehasbeennounanimousviewpointuponthelocationo…  相似文献   

18.
Objective Angiotensin Ⅱ (Ang Ⅱ ) contributes to modulating blood pressure by stimulation of Ang Ⅱ AT1 receptors. We devised a rat transient middle cerebral artery occlusion (MCAO) model to assess whether oxidative damage is decreased after pretreatment with Angiotensin Ⅱ AT1 receptor blocker (ARB). Methods After 2 weeks pretreatment with ARB 0. 5 and 1 mg/kg, the male Wister rats were subjected to 2 h middle cerebral artery occlusion (MCAO). At 24 h, the lumen diameter of middle cerebral artery, the plasma level of 8-hydroxy-2'-deoxyguanosine (8-OHdG), and HIF-1 a levels were recorded and compared. Results After pretrcatment with ARB 0.5 and 1 mg/kg, blood pressure did not significantly change compared with that of controls. In the group of candesartan at 1 mg/(kg· day), the lumen diameter was significantly increased compared to that in control group [(86.0±5.0) μm vs. (69.0± 2.1) μm; P<0. 01, n = 6- 8]. The plasma 8-OHdG levels of ARB pretreatment groups were decreased. In immunohistochemical findings, 8-OHdG- and HIF-1α-containing cells in ARB pretreatment groups were decreased. Conclusion Brain ischemia and oxidative damage can be reversed by AT1 receptor blockade in normotensive rats after transient cerebral artery occlusion.  相似文献   

19.
褪黑素对心理应激大鼠胃黏膜SOD、MDA和胃黏膜损伤的影响   总被引:10,自引:0,他引:10  
目的 探讨褪黑素 (MT)对心理应激性胃黏膜损伤的保护作用及其机制。方法  48只雄性SD大鼠随机分为对照组 (C组 )、规则光组 (R组 )、不规则光组 (I组 )和褪黑素组 (M组 )。检测大鼠胃黏膜损伤指数 (UI) ,胃黏膜超氧化物歧化酶 (SOD)活性、丙二醛 (MDA)含量及血清皮质醇浓度。结果 C组大鼠胃黏膜光整完好 ,肉眼未见糜烂及溃疡。R和I组UI均高于C组 (P <0 .0 5) ,M组UI低于I组 (P <0 .0 5)。R、I组胃黏膜SOD活性降低 ,I组降低更明显 (P <0 .0 5) ;R、I组胃黏膜MDA含量升高 ,I组升高明显 (P <0 .0 5) ,但M组SOD升高 ,MDA含量下降 (P <0 .0 5)。R、I组大鼠血清皮质醇升高 ,I组明显升高 (P <0 .0 5) ;而M组血清皮质醇较I组降低 (P <0 .0 5)。结论 褪黑素通过其抗氧化及抑制血清皮质醇水平的作用对心理应激性胃黏膜损伤起保护作用  相似文献   

20.
用细胞培养技术,观察了中药川芎嗪对培养脑微血管内皮细胞间粘附分子(IntercellularAdhesionMolecule-1,ICAM-1)表达的影响。细胞因子肿瘤坏死因子(TNF-α)和脂多糖(LPS)作用24h,使内皮细胞ICAM-1表达上调,预先用中药川芎嗪注射液处理3Omin,再用相同的细胞因子刺激,ICAM-1表达不升高。提示川芎嗪可抑制TNF-α和LPS引起的ICAM-1表达增加。  相似文献   

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