大鼠实验性心肌梗塞时血浆蛋白C,纤溶活性变化及人参皂甙作用的研究

通过观察实验性大鼠急性心肌梗塞（ＡＭＩ）时血浆蛋白Ｃ（ＰＣ）活性和组织型纤溶酶原激活剂（ｔ－ＰＡ）及纤溶酶原激活剂的特异性抑制因子（ＰＡＩ）活性的变化，初步探讨了心肌缺血时ＰＣ活性变化与纤溶系统的关系以及人参皂甙对其变化的影响。结果表明，１．ＡＭＩ时血浆ＰＣ活性显著低于正常对照组，且与缺血程度呈负相关。２．ＡＭＩ时ｔ－ＰＡ活性降低，ＰＡＩ活性增高。３．人参皂甙可提高ＡＭＩ时血浆ＰＣ活性，降低ＰＡＩ     

卡托普利对家兔急性心肌梗塞早期血小板活化及纤溶活性的影响

本研究观察了家兔急性心肌梗塞（ＡＭＩ）早期血浆血小板α－颗粒膜蛋白（ＧＭＰ－１４０）、血栓素Ｂ２（ＴＸＢ２）、组织型纤溶酶酶原激活剂（Ｔ－ＰＡ）及其抑制物（ＰＡＩ－１）水平的变化及卡托利干预的ＰＡ活性显著降低；相关分析表明，血浆ＧＭＰ－１４０浓度与ＰＡＩ－１活性显著正相关。卡托普利干预后，血浆ＧＭＰ－１４０浓度、ＴＹＸＢ２浓度、Ｔ－ＰＡ浓度、ｔ－ＰＡ含量、ＰＡＩ－１活性均明显降低，而ｔ－ＰＡ活性显     

血浆内皮素—1和肿瘤坏死因子与急性心肌梗塞的关系

本文对２０例急性心肌梗塞（ＡＭＩ）患者检测了血浆内皮素－１（ＥＴ－１）和肿瘤坏死因子（ＴＮＦ）的水平，结果表明，ＡＭＩ组的ＥＴ－１、ＴＮＦ均较正常对照明显升高（Ｐ〈０．００１），且二者与肌酸磷酸激酶的ＭＢ同功酶（ＰＣＫ－ＭＢ）均呈正相关（ｒ＝０．０６９８４，Ｐ〈０．００１；ｒ＝０．６０５３，Ｐ〈０．０１）。研究结果说明ＥＴ－１和ＴＮＦ参与了ＡＭＩ的病理损伤过程。     

过敏性哮喘豚鼠血小板激活因子的变化及川芎嗪的影响

本研究采用生物定量测定方法观察了豚鼠实验性哮喘时血浆ｌｙｓｏ－ＰＡＦ和肺泡灌洗（ＢＡＬＦ）中ＰＡＦ的变化。结果显示：致敏级豚鼠哮喘发作时血浆ｌｙｓｏ－ＰＡＦ水平显著高于对照组（Ｐ〈０．０１），ＢＡＬＦ中ＰＡＦ水平也明显高于对照组（Ｐ〈０．０５），同时伴有血浆及ＢＡＬＦ中ＴＸＢ２、ＴＸＢ２／６－酮－ＰＧＦ１α水平的升高（Ｐ〈０．０１）。致敏＋川芎嗪组豚鼠血浆ｌｙｓｏ－ＰＡＦ明显低于致敏组豚鼠（Ｐ〈０     

慢性阻塞性肺病患者血浆内皮素水平与肺血流动力学的关系

本文报告采用放射免疫方法测定慢性阻塞性病２４例（ＣＯＰＤ）患者体静脉，肺动脉，体动脉血的血浆ＥＴ－１水平，并与１６例正常对照组作了比较，ＣＯＰＤ患者尚进行了肺动脉压力直接测定，结果表明，ＣＯＰＤ患者ＥＴ－１水平显著高于正常组（Ｐ〈０．００１），肺动脉高压（ＰＡＨ）组ＥＴ－１水平显著高于ＰＡＨ组（Ｐ〈０．０５）。本文还分参与ＣＯＰＤ患者血浆ＥＴ－１水平的升高在ＰＡＨ形成可能是参与发病的因素之定。血浆     

L-精氨酸对缺氧性肺动脉高压大鼠内皮素释放的影响

目的：探讨Ｌ－精氨酸（Ｌ－Ａｒｇ）对缺氧性肺动脉高压（ＨＰＨ）大鼠血浆内皮素－１（ＥＴ－１）释放的影响。方法：将Ｗｉｓｔａｒ大鼠４０只分为：对照组,缺氧组,缺氧＋Ｎ＾ω－硝基－Ｌ－精氨酸甲脂（Ｌ－ＮＡＭＥ）组和缺氧Ｌ－Ａｒｇ组。结果：缺氧组的肺动脉平均压（ｍＰＡＰ）显著高于对照组（Ｐ〈０．０５）,缺氧组＋Ｌ－Ａｒｇ组的ｍＰＡＰ显著低于缺氧组（Ｐ〈０．０５）及缺氧＋Ｌ－ＮＡＭＥ组（Ｐ〈０．０１）,缺     

家兔血液流变学参数及其影响因素

目的检测正常家兔血液流变学指标,建立其正常参考值,并对有关影响因素进行探讨。方法采用ＮＸＥ－１型锥板式粘度计。测定５．７５５~(－１)～３０７．２Ｓ~(－１)七个切变率的血液表观粘度、血浆粘度、红细胞硬度指数（ＴＫ）、红细胞聚集指数（ＲＡＩ）和氧释放系数（ＯＤ）。结果雄性组家兔高切变率和低切变率下的血液粘度及ＲＡＩ较雌性组明显增高（Ｐ<０．０５和Ｐ<０．０１）,而ＯＤ较雌性组明显降低（Ｐ< ０．０５）。高体重组家兔高、中、低各切变率下的血液粘度和红细胞压积（Ｈｃｔ）较低体重组明显增高（Ｐ< ０．０５和Ｐ<０．０１）,而ＯＤ明显低于低体重组（Ｐ<０．０５）。高Ｈｃｔ组家兔的血液粘度、ＯＤ较低Ｈｃｔ组明显增高（Ｐ均<０．０１）,而血浆粘度和ＴＫ较低Ｈｃｔ组明显降低（Ｐ＜０．０５和Ｐ<０．０１）。结论家兔不同性别、体重和Ｈｃｔ,其血液流变学指标存在明显差异。     

人参皂甙对大鼠心肌缺血再灌注时纤溶活性变化的影响

本文应用Ｌａｎｇｅｎｄｏｒｆｆ无作功循环式离体心脏灌流技术、结扎左冠脉前降支造成急性心肌梗塞模型，以冠脉流出液和血浆为标本，观察人参皂甙对缺血再灌注损伤时纤溶活性变化的影响。结果显示，离体心脏停灌４５ｍｉｎ或再灌１５ｍｉｎ后，组织型纤溶酶原活化物（ｔ－ＰＡ）活性呈明显降低（与正常灌注相比Ｐ分别＜０．０５，０．０１），预灌注人参皂甙后，ｔ－ＰＡ活性可恢复到缺血以前的水平。人参皂甙２００ｍｇ／ｋｇ一次     

原发性肝癌患者血清可溶性细胞间粘附分子-1检测

应用酶联免疫吸附法检测了３８例原发性肝癌（ＰＨＣ）患者血清ｓＩＣＡＭ－１含量,结果表明：⑴ＰＨＣ患者血清ｓＩ ＣＡＭ－１水平明显高于健康对照,肿瘤直径≥５ｃｍ或结节≥３个组血清ｓＩ ＣＡＭ－１水平高于肿瘤直径〈５ｃｍ或结节〈３个组,静脉癌栓形成组（Ｐ均小于０．００１）;⑵ＰＨＣ患者血清ｓＩ ＣＡＭ－１水平与血清Ｂｉｌ－Ｔ、ＡＳＴ含量呈明显正相关（Ｐ〈０．０５）,而与血清ＡＦＰ含量无明显正相关（Ｐ〉     

高胆固醇血症大鼠LDL受体与apoA—1mRNA的水平变化及苯甲…

本文研究了实验性高胆固醇血症大鼠肝及小肠中低密度脂蛋白（ＬＤＬ）受体ｍＲＮＡ和载脂蛋白（ａｐｏ）Ａ－１ｍＲＮＡ的水平变化以及苯甲酸雌二醇（ＥＢ）对二者的影响。发现高脂（ＨＣ）组肝及小肠ＬＤＬ受体ｍＲＮＡ水平分别低于正常组５０％和６０％（Ｐ〈０．０５），小肠ａｐｏＡ－１ｍＲＮＡ水平低于正常组５８％（Ｐ〈０．０５），此时血清总胆固醇（ＴＣ）及ＬＤＬ胆固醇（ＬＤＬ－ｃ）均明显于正常组（Ｐ〈０．０１），血     

登革2型病毒调控血管内皮细胞纤溶系统相关蛋白的表达

目的观察登革2型病毒（DV2）对人脐静脉血管内皮细胞（HUVEC）表达组织纤溶酶原激活物（tPA）和纤溶酶原激活物抑制物1（PAI-1）的影响。方法应用胰酶消化分离HUVEC并进行传代培养，用生长良好的第2．3代细胞进行试验。用cell counting kit-8（CCK-8）测定DV2感染后细胞活性变化；发色底物法测定感染DV2组和对照组培养液中tPA、PAI-1活性；RT-PCR检测细胞内tPA和PAI-1 mRNA水平。结果DV2感染对细胞活力的影响与对照组相比差异无统计学意义。感染DV2组培养液中tPA活性在12～72h显著升高（P〈0．05）；DV2诱导HUVEC表达tPA mRNA的水平显著上调，12h达到峰值，以后渐降，72h mRNA表达水平仍高于对照组（P〈0．01）。而DV2感染组培养液中PAI-1活性和PAI-1 mRNA的表达与对照组比较差异无统计学意义（P〉0．05）。结论DV2感染可显著上调HUVEC的tPA mRNA转录，增强内皮细胞tPA蛋白的分泌，而不影响PAI-1 mRNA的转录或改变内皮细胞PAI-1的分泌。结果提示DV2可活化但并不损伤内皮细胞，诱发内皮细胞增强表达纤溶酶原激活物而致使纤溶系统失衡，引起纤溶亢进，这可能是诱发DHF／DSS患者急性期出血、低血容量性休克等体征的主要因素之一。     

代谢综合征患者纤溶活性与胰岛素抵抗的关系

目的:探讨代谢综合征患者血浆纤溶活性及与胰岛素抵抗的关系。方法:选择单纯代谢综合征患者36例,代谢综合征合并冠心病患者44例和健康人群对照20例。观察一般情况,并测定血浆纤溶酶原激活抑制物-1(PAI-1)和组织型纤溶酶原激活物(t-PA)、纤维蛋白原(Fib)、空腹血糖(FBG)、空腹血胰岛素(Ins)和血脂等指标;计算胰岛素敏感指数(ISI)。结果:代谢综合征患者的ISI较正常对照组明显下降(P<0.05);血浆PAI-1、Fib等明显升高(P<0.05)。代谢综合征合并冠心病组PAI-1与Fib、Ins正相关,与ISI、高密度脂蛋白(HDL)负相关。结论:代谢综合征患者存在明显的胰岛素抵抗和纤溶活性异常,同时纤溶活性异常与胰岛素抵抗相关。     

Pathways of fibrin turnover of human pleural mesothelial cells in vitro.

The mesothelium contains both procoagulant and fibrinolytic activities. An imbalance between these activities could account for the abnormal fibrin turnover and pleural fibrin deposition that is characteristic of pleural inflammation. Procoagulant activity of human pleural mesothelial cells (HPMC) is in part due to tissue factor, and the prothrombinase complex can also assemble at the HPMC surface. HPMC express tissue plasminogen activator (tPA) but no detectable fibrinolytic activity in a fibrin plate assay. Inhibition of HPMC fibrinolytic activity is due, in part, to elaboration of plasminogen activator inhibitors-1 and -2 (PAI-1 and PAI-2) as well as antiplasmins. Synthesis of PAI-1 and PAI-2 is inhibited by actinomycin D and cyclohexamide. HPMC PAI-1 is increased by transforming growth factor-beta (TGF-beta) and tumor necrosis factor-alpha (TNF-alpha), as is tPA release, while PAI-1 mRNA is unchanged and tPA mRNA is increased. PAI-2 release is induced by TNF-alpha and TGF-beta. Because they are a rich source of PAI-1 and PAI-2, HPMC may contribute to the high levels of these inhibitors in pleural exudates. Stimulation of HPMC by TNF-alpha or TGF-beta in vitro did not alter HPMC procoagulant activity nor the balance of elevated PAI and antiplasmins relative to PA, changes that collectively favor formation and persistence of pericellular fibrin.     

Fibrinolytic activity is not dependent upon exercise mode in post-myocardial infarction patients

In this study we investigated possible differences in fibrinolytic activity in cardiac patients while they performed treadmill and cycle ergometry. Thirteen post-myocardial infarction patients completed two maximal exercise tests on treadmill and cycle ergometers. Blood was collected before and after each exercise test and was analyzed for the fibrinolytic variables, tissue plasminogen activator (t-PA) and plasminogen activator inhibitor-1 (PAI-1) activity, and lactate. Maximal oxygen uptake, heart rate, and ventilation were greater (P?P?相似文献   

Glycaemic control, smoking habits and diabetes duration affect the extrinsic fibrinolytic system in type I diabetic patients but microangiopathy does not

The fibrinolytic system was studied in 43 type I diabetic patients with long duration of the disease, with or without evidence of microangiopathy, and in 26 control subjects. There were positive and independent correlations between tissue plasminogen activator (tPA) activity after venous occlusion and HbA1c, and between triglycerides and plasminogen activator inhibitor (PAI-1) and tPA antigen concentrations before and after venous occlusion. The tPA activities both at rest and after venous occlusion were higher in the patients. There were no differences with regard to sex, hypertension or nephropathy for the levels of fibrinolytic variables in these patients. Subjects with retinopathy did not differ from those without retinopathy. Diabetes duration showed a significant negative association with tPA activity in multivariate regression analysis. Tobacco-smoking diabetics, as compared to non-smoking, had an increased tPA antigen release at venous occlusion, but also higher PAI-1 levels and reduced specific activity of the tPA protein. When assessed with the new specific assays now available, the fibrinolytic parameters appear to be specific indicators of endothelial dysfunction related to smoking and to degree of glycaemic control in type I diabetic subjects.     

LPS促进HUVECs表达纤溶酶原激活物抑制物1

目的：观察LPS对脐静脉血管内皮细胞(HUVECs)表达组织纤溶酶原激活物(tPA)和纤溶酶原激活物抑制物1(PAI-1)的影响。 方法： 用生长良好的第2、3代HUVECs进行试验。用cell counting kit-8(CCK-8)测定LPS刺激后细胞活性变化；发色底物法测定LPS组和对照组培养液中tPA, PAI-1活性；RT-PCR检测细胞内tPA和PAI-1 mRNA水平。 结果： 与对照组相比，LPS(10 mg/L)对细胞活性没有明显差异。LPS诱导PAI-1活性在24-72 h显著升高(P<0.05),且显著上调PAI-1 mRNA，24 h达到峰值，以后渐降，72 h达到正常水平。而LPS组与对照组tPA活性与tPA mRNA无明显差异(P>0.05)。 结论： LPS(10 mg/L)可显著上调PAI-1 mRNA转录和分泌而不影响tPA mRNA，结果提示LPS可活化内皮细胞，诱发PAI-1 mRNA表达和蛋白分泌而抑制纤溶系统，这有利于微血栓的形成、血栓稳定,血液凝固和DIC发生。     

Association between platelet activation and fibrinolysis in acute stroke patients

We aimed to evaluate platelet activation and fibrinolyis in acute atherosclerotic ischemic stroke patients to clarify the relationship between them. Plasma P-selectin antigen, tissue plasminogen activator (tPA) antigen and activity, and plasminogen activator inhibitor-1 (PAI-1) activity were determined in 60 acute atherosclerotic stroke patients and matched control subjects. All patients were examined within 72 h after stroke onset. The levels of P-selectin, tPA antigen, and PAI-1 activity were all significantly higher in stroke patients compared with controls (all p < 0.0001); the level of tPA activity was significantly lower in patients than that in controls (p < 0.0001). These markers did not change much at different time points within 72 h. In stroke group, P-selectin concentration was highly correlated to PAI-1 activity (r = 0.8433, p < 0.001), but not to tPA antigen (r = -0.1752, p > 0.05), and tPA activity (r = 0.2465, p>0.05), which was further confirmed in the multiple linear regression analysis (F = 47.052, p < 0.0001). Our results indicate increased platelet activation and decreased fibrinolysis in patients with acute atherosclerotic ischemic stroke. Increased platelet activation may be correlated with decreased fibrinolysis.     

Neutralizing the neurotoxic effects of exogenous and endogenous tPA

The clinical use of tissue-type plasminogen activator (tPA) in the treatment of stroke is profoundly constrained by its serious side effects. We report that the deleterious effects of tPA on cerebral edema and intracranial bleeding are separable from its fibrinolytic activity and can be neutralized. A hexapeptide (EEIIMD) corresponding to amino acids 350-355 of plasminogen activator inhibitor type 1 (PAI-1) abolished the tPA-induced increase in infarct size and intracranial bleeding in both mechanical and embolic models of stroke in rats, and reduced brain edema and neuronal loss after traumatic brain injury in pigs. These experiments suggest mechanisms to reduce the neurotoxic effects of tPA without compromising its fibrinolytic activity, through the use of selective antagonists and new tPA formulations.     

Acute psychological stress decreases plasma tissue plasminogen activator (tPA) and tissue plasminogen activator/plasminogen activator inhibitor-1 (tPA/PAI-1) complexes in cardiac patients

Tissue plasminogen activator (tPA) promotes fibrinolysis, and impaired fibrinolysis is associated with atherosclerosis and thrombosis. Plasminogen activator inhibitor-1 (PAI-1) inhibits t-PA expression. The effects of acute laboratory stressors on tPA and tPA/PAI-1 complexes were assessed in a sample of 11 cardiac patients. Participants were randomly assigned to either a stress or relaxation condition at time 1, and the alternative condition at time 2. Blood samples were taken before (pre) and after (post) each session and participants completed a battery of psychological questionnaires. Two-way repeated-measures analysis of variance revealed a statistically significant decrease in tPA (P=0.01) and tPA-PAI-1 complexes (P=0.04) during the mental stress condition. Anger-in had a strong relationship to decreases in tPA/PAI-1 levels in the stress condition (r=0.68, P?<?0.05). Relaxation had no significant effect on tPA and tPA/PAI-1 levels. These data suggest that decreased fibrinolysis mediates the relationship between mental stress and atherosclerosis.     

Hormonal regulation of tissue-type plasminogen activator and plasminogen activator inhibitor type-1 in cultured monkey Sertoli cells

Sertoli cells play a central role in the control and maintenanceof spermatogenesis. Isolated Sertoli cells of mouse and rattestes have been shown to secrete plasminogen activator (PA)and a plasminogen activator inhibitor type-1 (PAI-1) in culture.In this study, we have investigated the hormonal regulationof PA and PAI-1 activities in cultured monkey Sertoli cells.Sertoli cells (5x10⁵ cells/well) isolated from infant rhesusmonkey testes were preincubated at 35°C for 16 h in 24-wellplates precoated with poly(D-lysine) (5 µg/cm²) in 0.5ml McCoy's 5a medium containing 5% of fetal calf serum and furtherincubated for 48 h in 0.5 ml serum-free medium with or withoutvarious hormones or other compounds. PA as well as PAI-1 activitiesin the conditioned media were assayed by fibrin overlay andreverse fibrin autography techniques respectively. The Sertolicells in vitro secreted only tissue-type PA (tPA), no detectableamount of urokinase-type PA (uPA) could be observed. MonkeySertoli cells were also capable of secreting PAI-1. Immunocytochemicalstudies indicated that both tPA and PAI-1 positive staininglocalized in the Sertoli cells, spermatids and residual bodiesof the seminiferous epithelium; Northern blot analysis furtherconfirmed the presence of both tPA and PAI-1 mRNA in monkeySertoli cells. Addition of follicle-stimulating hormone (FSH)or cyclic adenosine monophosphate (cAMP) derivatives or cAMP-generatingagents and gonadotrophin-releasing hormone (GnRH) agonist orphorbol ester (PMA) to the cell culture significantly increasedtPA activity. PAI-1 activity in the culture was also enhancedby these reagents except 8-bromo-dibutyryl-cAMP, forskolin and3-isobutyl-1-methylxanthin (MIX) which greatly stimulated tPAactivity, whereas decreased PAI-1 activity, implying that neutralizationof PAI-1 activity by the high level of tPA in the conditionedmedia may occur. These data suggest that increased intracellularsignals which activate protein kinase A (PKA), or protein kinaseC (PKC) can modulate Sertoli cell tPA and PAI-1 activities.The concomitant induction of PA and PAI-1 by the same reagentsin the Sertoli cells may reflect a finely tuned regulatory mechanismin which PAI-1 could limit the excession of the proteolysis. plasminogen activator inhibitor type-1/Rhesus monkey/Sertoli cells/tissue-type plasminogen activator