正常人静脉血流阻断后血浆组织型纤溶酶原激活剂含量、活性及其抑制物活性的变化

用酶联免疫吸附法(ELISA)和比色分析法测定了20名正常人血浆组织型纤溶酶原激活剂(Tissue plasminogen activator,tPA)的含量、活性及纤溶酶原激活剂抑制物(Plasminogen activator inhibitor,PAI)的活性。检测到正常人在静脉血流阻断后,血浆tPA含量、活性均有显著增高,PAI活性变化不大。讨论了血浆tPA和PAI测定的临床意义。     

高血压患者凝血、纤溶活性变化及硝苯地平缓释剂对它的影响

OBJECTIVE: To investigate the changes of coagulation and fibrinolysis status in patients with essential hypertension (EH) and observe the therapeutic effect of sustained-release nifedipine. METHODS: Ninety-nine EH patients were divided according to their diastolic blood pressure (DBP) into mild group (48 cases), moderate group (29 cases) and severe group (22 cases), and 25 patients among the groups were chosen at random to receive sustained-release nifedipine for 2 weeks. Twenty healthy subjects served as control group. Plasma D-dimer (DD), fibrin monomer (FM) and tissue-type plasminogen activator (tPA) levels were determined in all the subjects by enzyme-linked immunosorbent assay (ELISA). RESULTS: The plasma DD and FM levels were much higher, while tPA level was much lower in hypertensives than those of normal controls, exacerbating with the severity of the disease. DBP was positively correlated with plasma FM level (r=0.374,P<0.001). In patients with left ventricular hypertrophy, left ventricular enlargement and left atrial enlargement, higher levels of DD, FM and tPA were detected. Nifedipine treatment produced significant reduction in plasma DD and FM levels along with the increase in tPA level [DD: (40.7+/-23.5) mg/dl vs (23.8+/-16.5) mg/dl; FM: (7.0+/-1.6) ng/microliter vs (4.8+/-1.5) ng/microliter tPA: (0.31+/-0.14) ng/ml vs(0.41+/-0.05) ng/ml, P<0.001]. CONCLUSION: Enhanced coagulative activity and lowered fibrinolytic activity characterize EH patients and nifedipine may correct this disorder.     

健康人纤溶活性与年龄、性别、体重、血脂及吸烟习惯的相关性

对１０４名健康人血浆组织型纤溶酶原激活物（ｔＰＡ）和１３１名健康人血浆纤溶酶原激活物抑制物１（ＰＡＩ１）活性与年龄、性别、体重、血脂及吸烟习惯的关系进行了分析。结果表明：ＰＡＩ１活性随年龄及体重指数增加而增加;男性ＰＡＩ１与年龄、体重呈正相关;女性ＰＡＩ１与ＬＤＬ呈正相关;吸烟组ＰＡＩ１／ｔＰＡ值高于不吸烟组。提示年龄、体重、血脂参与调节纤溶活性,吸烟降低纤溶功能     

冠心病患者冠状动脉介入治疗前后tPA和PAI的变化

目的观察冠心病患者行冠状动脉介入治疗（PCI）手术前后血浆组织型纤溶酶原激活物（tPA）及纤溶酶原激活抑制剂（PAI）的动态变化。方法采用ELISA法对50例冠心病患者在PCI（包括PTCA和冠脉支架植入）手术前、手术后即刻和手术后4 d测定血浆中tPA和PAI的活性,并将冠心病患者的tPA、PAI浓度和tPA/PAI比值进行比较。结果冠心病患者tPA活性较正常对照组明显降低,PAI活性明显增高,在PAI手术后即刻tPA活性较手术前明显降低,但术后4 d回升,较正常对照组仍然明显降低,较PCI手术前无明显差异 冠心病患者PAI活性在PCI手术后明显升高,与手术前比较具有明显差异性,但术后4 d下降,,较PCI手术前无明显差异,但仍高于正常对照组。结论冠心病患者PCI手术存在着内皮损伤,导致手术后出现纤溶功能降低,而纤溶功能的低下会影响PCI的治疗效果。     

急性心肌梗塞患者血浆t-PA及其抑制物变化的临床研究

应用发色底物法测定急性心梗(AMI)患者入院当天、第7天及第14天的血浆组织纤溶酶原激活物(t-PA)及其抑制物(PAI)的活性变化。结果表明:PAI活性在AMI急性发作期及稳定期持续显著高于对照组,而t-PA活性在入院当天明显降低,但于第7天后回升接近于正常水平。再发性心梗患者的t-PA活性明显低于对照组及初发性心梗患者,急性期死亡患者的PAI活性明显升高而t-PA活性极度降低。PAI活性在CPK峰值不同的亚组中无显著差异,提示AMI患者存在着纤溶活性受损,高水平的PAI活性不是一种组织损伤非特异性的急性期反应。     

纳豆素对大鼠腹主动脉血栓形成的抑制作用

目的 :在复制大鼠血栓模型上 ,通过动态观察血压的变化、比较血栓的大小以及检测纤溶酶原激活物抑制物 (PAI)、组织型纤溶酶原激活物 (tPA)活性等指标 ,观察纳豆素的溶栓效应。方法 :S -D大鼠随机分五组 (n =40 ) ,用不同浓度的纳豆素灌胃 ,同等剂量的蚓激酶设为阳性对照 ,用Powerlab/ 4s生理多导仪描记股动脉血压 ,血栓干重用考马斯亮蓝法蛋白定量 ,采用酶联免疫法测定血浆中PAI及tPA活性。结果 :纳豆素组与对照组、单纯血栓组相比 ,复制血栓前血压无显著性差异 (P >0 .0 5) ,血栓复制后 40min ,纳豆素组、蚓激酶组血压下降幅度 (-1 1 .62± 7.36 %、- 8.37± 1 0 .2 9%、- 7.2 8± 4 .54 % )与单纯血栓组血压下降幅度 (- 59.97± 1 2 .2 9% )相比具有显著性差异 (P <0 .0 1 ) ;纳豆素处理的动物与单纯血栓组动物比较 ,其血栓的湿重、干重、蛋白含量显著性降低 (P <0 .0 1 ) ;纳豆素组、蚓激酶组血浆中tPA活性升高 ,PAI/tPA比值与对照组相比显著降低 (P <0 .0 1 )。结论 :纳豆素抑制动脉血栓的形成 ,提高纤维蛋白溶解活性     

葛根素对不稳定型心绞痛病人胰岛素抵抗及纤溶活性的影响

①目的　探讨葛根素对不稳定型心绞痛 (UA)病人胰岛素抵抗 (IR)及纤溶活性异常的影响。②方法6 9例UA病人随机分为常规治疗组 (31例 )和葛根素治疗组 (38例 ,于常规治疗基础上加用葛根素治疗 ) ,均于治疗前及治疗结束时检测血糖、血浆胰岛素 (FINS)、纤溶指标 ,计算胰岛素敏感性指数 (ISI)。选择 30例健康人作为对照组。③结果　与对照组比较 ,UA组FINS浓度增高 ,ISI降低 ,组织型纤溶酶原激活物 (tPA)活性降低 ,纤溶酶原激活物抑制物 1(PAI 1)活性升高 (t=2 .139～ 3.2 0 7,P <0 .0 5 ,0 .0 1)。葛根素组治疗后 ,FINS浓度降低 ,ISI增高 ,tPA活性增高 ,PAI 1活性下降 (t=2 .116～ 3.6 36 ,P <0 .0 5 ,0 .0 1)。UA组治疗前及葛根素组治疗后FINS ,ISI与PAI 1之间存在高度线性相关 (r =0 .35 1,- 0 .332 ,0 .4 2 7,- 0 .4 5 2 ,P <0 .0 1)。④结论　葛根素可改善UA病人的IR及与IR密切相关的纤溶活性异常。     

冠心病心绞痛病人血浆t—PA及其抑制物活性的测定

①目的探讨冠心病心绞痛病人血浆组织型纤溶酶原激活物(t-PA)及其抑制物(PAI)活性的变化及其可能机制.②方法采用显色底物法对20例冠心病心绞痛病人和20例健康人血浆t-PA及PAI的活性进行测定.③结果心绞痛病人血浆t-PA活性显著低于对照组(t=3.87,P＜0.01),PAI活性明显高于对照组(t=2.63,P＜0.05),65岁以上老年病人上述指标的异常变化尤为显著(t=3.87,2.98,P＜0.01).④结论冠心病心绞痛病人存在纤溶系统功能异常,有可能在冠状动脉粥样硬化的基础上形成血栓.     

Clinical studies on treatment of acute cerebral infarction with Xueshuantong injection

Objective: To observe the effect of Xueshuantong injection (XST, with its ingredient as Notoginseng saponin, on acute cerebral infarction (ACI) and on blood coagulation and fibrinolysis, so as to comprehensively analyse the mechanism of XST.Methods: Fifty ACI patients were randomly divided into 2 groups, and XST group (30 patients) was treated with XST, and the control group (20 patients) given low molecular dextrose, as well as low molecular heparin calcium. The course of treatment for both groups was 15 days. The changes of effective rate, score of neurologic impairment, tissuetype plasminogen activator (tPA), inhibitor of plasminogen activator (PAI), D-D dimmer, antithrombinIII (AT-III), and fibrinogen (Fbg) were all observed.Results: The total effective rate of XST group was 73.33%, that of the control group 65. 00%. After the therapy, plasma level of tPA, ratio of tPA/PAI, and AT-III content were increased obviously, while the plasma level of PAI and D-D dimmer were decreased significantly (all P<0.01). But there was only insignificant difference between the 2 groups (P> 0.05).Conclusion: XST injection could be effective to ACI, the mechanism of which is probably related to improving the balance between plasminogen activator and its inhibitory factor, increasing the activity of fibrinolysin, inactivating thrombin, inhibiting platelet aggregation induced by thrombin, and decreasing blood coagulation.     

抑肽酶对心脏直视手术患者血液纤溶活性的影响

作者对25例抑肽酶组和对照组体外心脏直视手术患者进行了术前、术后血液纤溶酶原抗原(Plg)、纤溶酶活性(Plm)、组织纤溶酶原活化素(tPA)、纤溶酶原活化素抑制物(PAI)及D-二聚体(D-D)的研究。发现对照组术后Plg、Plm及PAI较术前明显降低(P<0.005、P<0.001及P<0.05);tPA、D-D明显增加(P<0.005、P<0.001)。抑肽酶组除tPA较术前明显降低外(P<0.005),其余各项指标亦明显增加,但术后抑肽酶组tPA、D-D明显低于对照组(P<0.005、P<0.05),而PAl明显高于对照组(P<0.005)。表明体外循环时纤溶活性增加,抑肽酶能抑制tPA、促进PAI的活性,从而抑制纤溶活性。     

New markers of bone and collagen turnover in children and adults with growth hormone deficiency.

Serum bone Gla protein (BGP), a marker of osteoblastic function, serum carboxyterminal cross-linked telopeptide of type I collagen (ICTP), a marker of bone resorption, and serum aminoterminal propeptide of type III procollagen (PIIINP) levels, an index of collagen synthesis, were determined in seven children and eight adults with congenital growth hormone deficiency (GHD). In children with GHD, serum BGP (mean +/- s.e.: 12.9 +/- 0.7 ng/ml), ICTP (8.3 +/- 1.3 ng/ml) and PIINP (3.5 +/- 0.5 ng/ml) levels were significantly lower (P < 0.001) than those recorded in normal children (BGP 18.9 +/- 0.8 ng/ml, ICTP 14.4 +/- 0.5 ng/ml and PIIINP 6.7 +/- 0.7 ng/ml). Total alkaline phosphatase (184.7 +/- 13.4 IU/l) and bone alkaline phosphatase (77.8 +/- 4.1 IU/l) levels were also significantly lower (P < 0.0001) than in controls (338.1 +/- 14.9 IU/l and 181.0 +/- 7.8 IU/l, respectively). Serum BGP, ICTP and PIIINP levels were not significantly correlated with height velocity values. In adults with GHD, mean BGP levels (3.8 +/- 0.3 ng/ml) were significantly lower (P < 0.0001) than those recorded in normals (5.4 +/- 0.1 ng/ml). On the contrary, serum ICTP levels were similar to those found in controls (patients: 4.7 +/- 0.8 ng/ml vs normals: 4.1 +/- 0.3 ng/ml), suggesting the presence of a normal resorption activity associated with a reduced osteoblastic function. This finding was also confirmed by the presence of reduced bone alkaline phosphatase levels (GHD: 44.9 +/- 6.9 IU/I vs controls: 58.3 +/- 2.0 IU/I; P<0.02), while the less specific total alkaline phosphatase levels (119.5 +/- 14.8 IU/I) were similar to those recorded in normal subjects (122.3 +/- 4.0 IU/I). Serum PIIINP levels (3.7 +/- 0.6 ng/ml) were similar to those recorded in normals (3.2 +/- 0.2 ng/ml), suggesting that in adulthood the collagen turnover is not negatively influenced by the chronic GHD. No significant correlations were found between BGP/ICTP/PIIINP and IGF-I levels. In conclusion, our data show that in children with GHD the lack of GH insulin-like growth factor-I (IGF-I) effects on bone and collagen turnover is associated with a significant reduction of bone turnover (low bone formation plus low bone resoRption) and collagen synthesis. On the contrary, adult GHD seems to exert less relevant effects on bone and collagen turnover, probably due to the fact that in adult life further hormones or local factors might partially counteract the negative consequences of chronic GH-IGF-I deficiency.     

急性脑梗死患者血浆尿激酶型纤溶酶原激活物及其受体的表达

目的　检测急性脑梗死患者血浆中尿激酶型纤溶酶原激活物 (uPA)及其受体 (uPAR)的含量变化 ,并探讨其在脑梗死发生发展过程中的作用。方法　应用ELISA双抗体夹心法分别测定89例急性脑梗死患者、30例其他疾病对照组和 30名健康对照组血浆中uPA和uPAR含量 ,并按病情分轻、中、重 3组进行比较。结果　脑梗死患者急性期血浆uPA和uPAR含量分别为 ( 16 6 4± 384 )ng/L及 ( 1375± 30 3)ng/L ,其他疾病对照组为 ( 10 33± 12 3)ng/L及 ( 978± 12 0 )ng/L ,正常对照组为 ( 10 0 5±12 9)ng/L及 ( 90 5± 15 9)ng/L。脑梗死组与后两组比较P <0 0 5或P <0 0 1。脑梗死患者恢复期uPA含量为 ( 1186± 385 )ng/L ,与两对照组比较P >0 0 5 ,uPAR含量为 ( 115 9± 2 6 1)ng/L ,明显高于两对照组 (均P <0 0 1)。重度患者急性期血浆uPA和uPAR含量分别为 ( 1939± 2 5 7)ng/L及 ( 15 11± 379)ng/L ,中度患者分别为 ( 15 94± 2 0 5 )ng/L及 ( 12 97± 15 1)ng/L ,轻度患者分别为 ( 135 9± 176 )ng/L及 ( 12 2 7± 98)ng/L ,重度患者组与后两组比较P <0 0 1;恢复期uPA和uPAR含量分别为 ( 115 3± 170 )ng/L及( 1186± 15 8)ng/L ,轻度患者分别为 ( 10 4 2± 187)ng/L及 ( 10 5 4± 10 9)ng/L ,两者比较P <0 0 5和     

老年抑郁症患者治疗前后血浆脑源性神经营养因子和组织纤维蛋白溶酶原激活物水平的变化

目的 探讨老年抑郁症患者治疗前后血浆脑源性神经营养因子(Brain-derived neurotrophic factor,BDNF)和组织纤维蛋白溶酶原激活物(tissue-type plasminogen activator,tPA)水平的变化,为老年抑郁症的诊断和治疗提供生物学指标.方法 用酶联免疫吸附法(ELISA)测定28例老年抑郁症患者冶疗前后和30例正常对照组血浆中BDNF和tPA的水平,使用汉密尔顿抑郁量表(Hamilton Depression Rating Scale,HDRS)评分反映抑郁严重程度.结果 与对照组[(958.83±150.20)pg/ml]比较,治疗前老年抑郁症患者血浆BDNF水平[(864.23±198.41)pg/ml]明显降低(P<0.05),治疗后血浆BDNF水平[(929.99±150.90)pg/ml]有升高趋势;患者组治疗前[(13.33±5.35)ng/ml]、治疗后[(11.83±5.02)ng/ml]及正常对照组[(12.53±5.35)ng/ml]间tPA水平差异无显著性(P>0.05);治疗前血浆BDNF和tPA之间相关无显著性.结论 BDNF可以作为老年抑郁症的一个生物学标记,tPA与BDNF之间可能存在复杂的中间调节过程.     

糖尿病肾病纤溶酶原激活物抑制因子-1检测分析

目的:探讨糖尿病肾病患者血浆纤溶酶原激活物抑制物的变化。方法:检测33例糖尿病肾病患者及30例健康体检对照组血浆纤溶酶原激活物抑制物-1(PAI-1),观察检测结果。结果:33例糖尿病肾病患者纤溶酶原激活物抑制物-1(PAI-1)检测值(51.7±12.5)ng/ml,明显高于对照组检测值(27.1±11.2)ng/ml(P<0.01)。结论:糖尿病肾病患者存在血浆纤溶酶原激活物及其抑制物系统失衡。     

Analysis of Plasma Fibrinolysis in the Patients with Acute Cerebral Infarction

ＡｎａｌｙｓｉｓｏｆＰｌａｓｍａＦｉｂｒｉｎｏｌｙｓｉｓｉｎｔｈｅＰａｔｉｅｎｔｓｗｉｔｈＡｃｕｔｅＣｅｒｅｂｒａｌＩｎｆａｒｃｔｉｏｎＺＨＡＮＧＹｉｎｇ－ｄｏｎｇ（张颖冬）；ＬＩＵＸｉ－ｍｉｎ（刘锡民）；ＣＡＩＺｈｕａｎ（蔡转）；ＹＡＮＧＭｉｎｇ－...     

氯沙坦对高血压患者纤溶活性和内皮血管活性物质的影响

目的 观察氯沙坦治疗原发性高血压(EH)时对纤溶活性、内皮素、一氧化氮、降钙素基因相关肽的影响.方法 48例健康体检者作为正常对照组,68例EH患者用氯沙坦治疗8周,观察用药前后血t-PA、PAI活性,ET、NO、CGRP浓度的变化.结果 EH患者t-PA活性、CGRP和NO浓度明显低于正常对照组(P<0.01),而P...     

老年高血压病患者血浆纤溶活性与胰岛素敏感性分析

采用发色底物法及放免法检测了３０例老年期高血压病（ＥＨ）患者和３０例健康老年人血浆组织型纤溶酶原激活物（ｔ－ＰＡ）、纤溶酶原激活物抑制因子（ＰＡＩ）。空腹血浆胰岛素（Ｉｎ）、血糖（Ｇ）水平，分析了纤溶活性与胰岛素敏感性（ＩＳ）的相关性。结果发现：ＥＨ患者血浆ＰＡＩ活性明显高于对照组，血浆ｔ－ＰＡ活性及ＩＳ明显低于对照组；ＩＳ与ＰＡＩ显著负相关，与ｔ－ＰＡ显著正相关。提示：纤溶活性异常与胰岛素抵抗共同在高血压的发生发展中起重要作用。     

尿激酶型纤溶系统在乳腺癌细胞侵袭中的作用

目的研究尿激酶型纤溶系统组分uPA、uPAR、tPA及PAI-1在人乳腺癌细胞侵袭中的作用。方法以3株具有不同侵袭转移能力的乳腺癌细胞株作为研究对象,应用RT?PCR方法比较纤溶组分在此3株细胞中的表达,牛奶板法检测细胞培养上清中的纤溶活性,用Boyden小室模型测定细胞侵袭能力。结果发现MDA-MB-231细胞表达较高水平的uPA、uPAR、PAI-1和中等水平的tPA,无血清培养上清中总纤溶活性和uPA纤溶活性最高;MDA-MB-435细胞表达较低水平的uPA和较高水平的tPA,但未测出uPAR和PAI-1的表达,无血清培养上清中总纤溶活性较高,主要是tPA活性;MCF-7细胞表达较低水平的uPAR和较高水平的PAI-1,但未测出uPA和tPA的表达,无血清培养上清中几乎没有纤溶活性。与纤溶活性相一致的是,Boyden小室模型实验结果发现MDA-MB-231在3株细胞中体外侵袭能力最强,MDA-MB-435次之,MCF-7则几乎无体外侵袭能力。经抗uPA和抗uPAR抗体预处理MDA-MB-231细胞,分别使侵袭能力下降83.1%和43.9%(P<0.05)。结论uPA和uPAR的活性与乳腺癌细胞的侵袭转移能力密切相关     

纤溶酶原激动抑制剂-1基因4G/5G多态性与冠心病

采用特异性引物多聚合酶链式反应方法 ,检测了 1 2 3例冠心病患者和 1 72例健康对照者的纤溶酶原激动抑制剂 1 (PAI 1 )基因 ,并同时测定血液PAI 1质量浓度和活性 ,体质量指数、胆固醇和三酰甘油 ,探讨了PAI 1基因4G/5G多态性与冠心病的相关性。结果显示 ,冠心病组的缺失型纯合子 4G/4G型 ( 47.2 %)明显多于对照组 ( 2 2 .1 %,P <0 .0 5) ,4G/4G组的PAI 1质量浓度〔( 40 .87± 0 .99) μg/L)〕和PAI活性〔( 750± 350 )U/L〕均高于 5G/5G组〔( 38.1 4± 1 .0 ) μg/L ,( 650± 2 70 )U/L ,P <0 .0 5〕。提示PAI 1基因 4G/5G多态性与PAI 1质量浓度及活性具有相关性 ,并与冠心病的发病过程有关     

急性心肌梗死大鼠血管紧张素Ⅱ对PAI-1和tPA表达的作用及其机制

目的:探讨急性心肌梗死(AMI)大鼠血管紧张素Ⅱ(AngⅡ) 经AngⅡ1型受体(AT1R)激活细胞外信号调节激酶(ERK)对纤溶酶原激活物抑制剂-1(PAI-1)和组织型纤溶酶原激活物(tPA)活性的调节作用.方法:24只健康SD大鼠,按随机数字表法随机分为假手术组(n=8)、AMI组(n=8)和特异性ERK上游激酶...