冠心病患者纤溶活性,血小板功能及内皮素在运动前后的变化？…

目的 研究冠心病患者在运动前后纤溶活性，血小板活化状态及血管内皮功能的变化。方法 根据冠状动脉造影结果，选择冠心病患者（ＣＨＤ组）３７例，分为单支及多支病变组，另选健康人２７例为对照组（Ｃ组），采用次极量运动试验观察上述部分指标在运动前后的变化，结果 （１）运动前，组织型纤溶酶原激活剂（ｔＰＡ）纤溶酶原激活剂抑制因子－１（ＰＡＩ－１）活性，血浆５－羟色胺（５－ＨＴ）水平及血小板５－ＨＴ２Ａ受体密度     

犬实验性冠状动脉痉挛对纤溶系统的影响

目的：冠状动脉痉挛（ＣＡＳ）可发生在正常或已有部分狭窄的冠状动脉粥样斑块处，但其对纤溶系统的影响及机制尚不清楚，本研究旨在对此探讨。方法：采用脑垂体后叶素湿敷于犬左冠状动脉前降支外诱发ＣＡＳ的模型。将１５只健康杂种犬随机分为①对照组；②ＣＡＳ组；③冠状动脉部分狭窄＋ＣＡＳ组，观察上述模拟病理状况前后纤溶系统的改变。实验资料用配对ｔ检验。结果：对照组各实验值与其对照值比较无统计学意义（Ｐ＞０．０５）；②组（２次）及③组诱发ＣＡＳ后，与其相应的对照值比较，两组血浆组织型纤溶酶原激活剂（ｔＰＡ）活性及③组的６－酮－前列腺素Ｆ１α水平均显著降低（Ｐ＜０．０１与Ｐ＜０．０５），两组血浆ｔＰＡ抑制物（ＰＡＩ）活性、凝血烷Ｂ２（血栓素Ｂ２，ＴＸＢ２）、肾素活性及③组血浆纤维蛋白原与血管紧张素Ⅱ水平均显著增加（Ｐ＜０．０５或Ｐ＜０．０１）；③组心电图的改变酷似变异性心绞痛和急性心肌梗死。结论：犬实验性ＣＡＳ可导致纤溶系统活性降低，其机制可能主要与血小板活化或内皮细胞损伤有关。     

灯盏细辛干预血小板、凝血功能对急性冠状动脉血栓形成后溶栓的影响

目的观察灯盏细辛干预血小板、凝血、纤溶等功能时对急性心肌梗塞溶栓治疗的影响。方法３０条麻醉犬制成急性冠状动脉血栓形成模型,随机分为三组：生理盐水组;尿激酶组;尿激酶＋灯盏细辛组。结果灯盏细辛能明显改善尿激酶溶栓后血小板聚集率、血小板血栓素Ｂ２（ＴＸＢ２）、６酮前列环素等方面的变化（Ｐ＜０．００１）,并且能升高血中组织型纤溶酶原激活物（ｔＰＡ）（Ｐ＜０．０１）、抗凝血因子Ⅲ（ＡＴⅢ）（Ｐ＜０．０５）浓度,降低纤溶酶原激活物的抑制物（ＰＡＩ）浓度（Ｐ＜０．００１）。结论灯盏细辛可能使急性冠状动脉血栓形成时应用尿激酶溶栓治疗的再通率增加,再闭塞减少。     

蚓激酶抗凝、纤溶的机制及其与组织型纤溶酶原激活剂的关系

目的探讨蚓激酶抗凝、纤溶机制及其与组织型纤溶酶原激活剂（ｔＰＡ）的关系。方法给正常和高凝大鼠口服蚓激酶胶囊（２５ｍｇ·ｍｌ１·１００ｇ１体重，３天）后测白陶土部分凝血活酶时间（ＫＰＴＴ）、凝血酶原时间（ＰＴ）、优球蛋白溶解时间（ＥＬＴ）、纤溶酶原含量和体外血栓形成的变化，以及体内血浆及体外培养的内皮细胞上清液中ｔＰＡ、ｔＰＡ抑制物（ＰＡＩ）活性的变化。结果正常和高凝大鼠口服蚓激酶后ＫＰＴＴ明显延长；ＥＬＴ明显缩短。体外血栓形成仪测定显示血栓长度、重量均明显减小。纤溶酶原含量明显降低。正常大鼠、高凝大鼠血浆ｔＰＡ活性升高（均为Ｐ＜００５），与纤溶酶原含量降低间呈明显负相关（ｒ＝－０８７２，Ｐ＜００５）。在大鼠肺微血管内皮细胞培养中加入蚓激酶（５０～２００ｍｇ／Ｌ）后，上清液中ｔＰＡ活性明显升高（Ｐ＜００１），呈量效依赖关系；但ＰＡＩ活性无明显变化。蚓激酶溶液中含有ｔＰＡ活性，其与药物浓度呈显著正相关（ｒ＝０８５８５，Ｐ＜００５）。结论蚓激酶能部分抑制内凝血途径，激活纤溶，后者又与ｔＰＡ活性升高有关     

高血压病患者血小板活化状态和纤溶活性的变化

目的观察高血压病患者血小板活化状态和纤溶活性的变化并用缓释异搏定、开博通降压治疗后观察上述指标的变化。方法采用发色底物法、放射免疫法检测对象为Ⅰ、Ⅱ期高血压病患者５０例、正常对照者２５例的组织型纤溶酶原激活剂（ｔＰＡ）及其抑制物（ＰＡＩ１）的活性，其中高血压病患者３０例、正常对照者１７例测定了活化血小板α颗粒膜蛋白（ＧＭＰ１４０）的含量。５０例高血压病患者中２１例接受缓释异搏定治疗，１９例用开博通治疗，疗程１２周。结果高血压病患者ＰＡＩ１活性、ＧＭＰ１４０含量较正常高，ｔＰＡ活性低于正常；缓释异搏定和开博通降压治疗１２周后，ＰＡＩ１活性、ＧＭＰ１４０含量下降，ｔＰＡ活性增强，与治疗前比，差异有显著性（Ｐ值分别＜００５，００１）。结论提示Ⅰ、Ⅱ期高血压病患者血小板活化功能增强，纤溶活性降低。缓释异搏定和开博通均能在降压治疗的同时改善高血压病患者异常的血小板活化和纤溶活性     

卡托普利对冠心病患者内源性纤溶系统活性的影响

目的探讨卡托普利对不稳定性心绞痛（ＵＡＰ）和急性心肌梗死（ＡＭＩ）患者内源性纤溶系统的影响及其临床意义。方法４０例ＡＭＩ和ＵＡＰ患者随机分为卡托普利组和对照组。采用发光底物显色方法,检测两组治疗前和治疗后第３、７、１４、２１天血浆组织型纤溶酶原激活剂（ｔＰＡ）及其抑制物（ＰＡＩ）的活性。结果治疗前血浆ｔＰＡ活性呈现正常人＞ＵＡＰ＞ＡＭＩ患者,ＰＡＩ活性则相反,而且ＡＭＩ与ＵＡＰ,ＵＡＰ和正常人同项比较均有显著性差异（Ｐ＜０．０１）。卡托普利组血浆ＰＡＩ活性降低,ｔＰＡ活性增强,与治疗前和对照组同期比较差异显著（Ｐ＜０．０５,０．０１）。结论卡托普利增强冠心病患者内源性纤溶系统活性。     

老年脑梗死患者血纤溶活性与血小板活化的关系

我们于１９９４年１１月～１９９５年１１月观察了老年脑梗死患者早期血浆血小板α颗粒膜蛋白１４０（ＧＭＰ１４０）、组织型纤溶酶原激活物（ｔＰＡ）及其抑制物１（ＰＡＩ１）水平的改变，旨在探讨老年脑梗死患者早期血纤溶活性与血小板活化的关系，为早期联合应...     

冠心病组织型纤溶酶原激活物及其抑制物的活性变化

冠心病组织型纤溶酶原激活物及其抑制物的活性变化邱建钱学贤刘映峰刘兰平我们比较了不同类型冠心病血浆组织型纤溶酶原激活剂（ｔＰＡ）和纤溶酶原激活剂抑制物（ＰＡＩ）活性的变化，并探讨ｔＰＡ和ＰＡＩ活性变化与冠状动脉（冠脉）病变范围和冠脉狭窄程度的关系。对象...     

急性心肌梗塞患者溶栓治疗期间纤溶活性和血小板功能的变化及其临床意义

观察２０例急性心肌梗塞（ＡＭ１）患者早期溶栓治疗期间纤溶活性及血小板功能的变化，以２２例常规治疗病人为对照。结果显示静注尿激酶（ＵＫ）完毕后即刻血浆组织型纤溶酶原激活物（ｔＰＡ）活性直线上升（Ｐ＜０．００１），纤溶酶原激活物抑制物（ＰＡ１）活性直线下降（Ｐ＜０．００１），但不到２４ｈ血浆ＰＡＩ活性反跳超过静注ＵＫ前水平。血小板功能，因入院后即给阿司匹林治疗而受抑制，但静注ＵＫ完毕后，血小板最大聚集率达峰值。以上的变化说明溶栓治疗期间血栓与溶栓过程并存。了解溶栓治疗期间溶栓与凝血的病理生理过程对提高溶栓治疗的成功率和预防血管再堵的处理有很大意义。     

卡托普利对冠心病患者内源性纤溶功能的影响

目的：冠状动脉粥样硬化性心脏病（冠心病）患者内源性纤溶功能紊乱与肾素—血管紧张素系统激活有关，但转换酶抑制剂能否改善这种功能紊乱尚不十分清楚，本文目的是研究此作用。方法：符合世界卫生组织冠心病不稳定性心绞痛诊断标准，６５％经选择性冠状动脉造影确定冠状动脉狭窄≥５０％的患者３４例，单盲随机分为卡托普利治疗组（１８例）及安慰剂对照组（１６例），４周治疗前、后检测血浆肾素活性、血管紧张素Ｉ、组织型纤溶酶原激活剂（ｔ－ＰＡ）及纤溶酶原激活剂抑制物（ＰＡＩ）含量与活性，两组间的参数比较采用ｔ检验。结果：４周后，治疗组的血浆血管紧张素Ｉ及ｔ－ＰＡ含量、ＰＡＩ活性均显著低于对照组（Ｐ＜０．０５或Ｐ＜０．０１，而ｔ－ＰＡ活性及纤溶活力则显著高于对照组（Ｐ＜０．０５或Ｐ＜０．０１）。结论：卡托普利可通过降低血浆血管紧张素Ｉ水平，改善冠心病患者内源性纤溶功能紊乱。本结果对预防冠状动脉内血栓形成有意义     

缬沙坦对兔急性心肌梗死血小板活化、纤溶活性和内皮血管活性物质的影响

目的　探讨缬沙坦对急性心肌梗死血小板活化、纤溶活性和内皮血管活性物质的影响。方法　新西兰大白兔30只 ,随机分为三组 ,每组 10只 , 组 :假手术组 , 组 :急性心肌梗死组 , 组 :缬沙坦组 ; 、 组分别结扎冠状动脉左室支中点后 4 h,取血分别测定血栓素 B2 (throm boxane B2 ,TXB2 )、6 -酮 -前列腺素 F1α(6 - Keto- prostaglandinF1α,6 - Keto- PGF1α)、内皮素 (Endothelin,ET)、一氧化氮 (Nitric oxide,NO)浓度以及组织型纤溶酶原激活剂 (tis-sue- type plasminogen activator,t- PA)和纤溶酶原激活剂抑制物 (Plasm inogen activator inhibitor,PAI)活性 ;摘取心脏 ,测定心肌梗死范围。结果　 、 组与 组比较 ,血浆 TXB2 、ET、NO浓度和 PAI活性显著升高 (P<0 .0 1) ,6 - Keto- PGF1α浓度、t- PA活性显著下降 (P<0 .0 1) , 组与 组比较 ,血浆 TXB2 、ET、NO浓度和 PAI活性明显降低 (P<0 .0 1) ,6 - Keto- PGF1α浓度、t- PA活性显著升高 (P<0 .0 1) ,梗死范围减小。结论　缬沙坦抑制急性心肌梗死早期血小板活化 ,改善纤溶活性 ,减少 ET和 NO的释放 ,缩小心肌梗死范围     

Clinical significance of plasminogen activator inhibitor activity in patients with exercise-induced ischemia

To assess the fibrinolytic system in patients with exercise-induced ischemia and its relation to ischemia and severity of coronary artery disease (CAD), 47 patients with CAD confirmed by results of coronary angiography underwent symptom-limited multistage exercise thallium-201 emission computed tomography. All patients with CAD had exercise-induced ischemia as assessed from thallium-201 images. Pre- and peak exercise blood samples from each patient and preexercise blood samples from control subjects were assayed for several fibrinolytic components and were also assayed for plasma adrenaline. The extent of ischemia was defined as delta visual uptake score (total visual uptake score in delayed images minus total visual uptake score in initial images) and the severity of CAD as the number of diseased vessels. In the basal condition, plasminogen activator inhibitor (PAI) activity was significantly higher in patients with exercise-induced ischemia as compared to control subjects (p less than 0.01), although there were no significant differences in other fibrinolytic variables between the two groups. Moreover, PAI activity in the basal condition displayed a significantly positive correlation with the extent of ischemia (r = 0.47, p less than 0.01). Patients with exercise-induced ischemia were divided into two groups (24 with single-vessel disease and 23 with multivessel disease). There were no significant differences in coronary risk factors, hemodynamics, or plasma adrenaline levels during exercise between single-vessel and multivessel disease except that delta visual uptake score was significantly higher in multivessel disease (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Increased plasminogen activator inhibitor antigen levels in diabetic patients with stable angina.

PAI-1 antigen, tPA antigen and thrombin - antithrombin III complexes (TAT) levels were measured in 10 males with stable angina and type-II diabetes mellitus and in 16 males with stable angina without diabetes or other risk factors (hyperfibrinogenaemia, hyperlipidaemia, diabetes, hypertension, smoking and obesity) known to increase PAI levels. Ten healthy men of equivalent age served as controls. Because only diabetics with coronary artery disease (CAD) showed a decreased fibrinolytic capacity, a second study was performed on the 16 non-diabetic CAD patients to determine whether submaximal workload induces significant changes of tPA and PAI levels. TAT levels were increased in CAD, and significantly so in the diabetic group. tPA levels were increased only in the CAD patients without diabetes. PAI levels were significantly increased in diabetic CAD patients (5.26 +/- 1.96 ng/ml) but not in the stable angina patients without diabetes (2.97 +/- 1.44 ng/ml). Immunologically-reactive tPA released after exercise was higher in the 16 CAD patients without diabetes than in controls. Our data could indicate that in stable angina without diabetes there is no chronic latent activation of the clotting system, with no impairment of fibrinolytic activity. On the other hand, the presence of diabetes mellitus seems to influence the fibrinolytic capacity in CAD, particularly increasing PAI levels.     

Evidence for increased levels of plasminogen activator inhibitor and tissue plasminogen activator in plasma of patients with angiographically verified coronary artery disease

We studied 234 consecutive patients who underwent coronary angiography because of severe angina pectoris. Tissue plasminogen activator (tPA), plasminogen activator inhibitor (PAI), and lipoprotein Lp(a) were measured in citrated plasma samples. The 214 patients showing significant coronary artery stenosis (greater than 50% reduction of luminal area in any of the great coronary arteries) had higher mean levels of tPA (P less than 0.001) and PAI (P less than 0.01) than a random population sample of similar age. PAI and tPA levels were higher in smokers than in either non-smokers or ex-smokers, and in patients with hypertension tPA was increased. Subjects with blood group A had a higher mean Lp(a) level than subjects with blood group O. There were positive correlations of PAI and tPA levels with serum triglycerides and with body mass index; Lp(a) correlated weakly with plasma fibrinogen concentrations. The findings suggest an impairment of the fibrinolytic system in patients with coronary artery disease, which offers a link between established risk factors and a plausible pathophysiological mechanism, namely thrombus turnover.     

Detection of impaired fibrinolytic activity in coronary artery disease--electrophoretic and immuno-blotting analysis of tissue plasminogen activator

In present study, we investigated the fibrinolytic activities and plasma antigen levels of tissue plasminogen activator (tPA) before or after a submaximal exercise in patients with coronary artery disease (CAD). We also investigated tPA phenotypes in plasma by electrophoretic and immuno-blotting analysis. Euglobulin fractions obtained from plasma were submitted to sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) followed by immunoblotting analysis. There were no differences in plasma antigen levels of tPA between the study group and controls before or after the exercise, however CAD patients showed lower fibrinolytic activities after the exercise than controls. SDS-PAGE followed by immuno-blotting with an antisera against human tPA revealed two bands at molecular weights (m.w.) of 70,000 and 120,000. The band at m.w. of 70,000 corresponded to free tPA and that of 120,000 was considered to be identical to a complex of tPA with its inhibitor. Furthermore, we found a decrease in free tPA in the patients with low fibrinolytic activities. From these results it was concluded that impaired fibrinolytic activities, probably due to decreased free tPA, observed in CAD patients, might be an important factor in the pathogenesis of CAD.     

缬沙坦和卡托普利对缺血再灌注纤溶活性、内皮血管活性物质的影响

目的　探讨缬沙坦和卡托普利对缺血再灌注纤溶活性、内皮血管活性物质的影响。方法　新西兰大白兔 6 0只 ,随机分为五组 ,每组 12只 , 组 :假手术组 , 组 :急性心肌梗死 (AMI)组 , 组 :缺血再灌注 (ischem ic reperfu-sion,IR)组 , 组 :IR+卡托普利组 , 组 :IR+缬沙坦组 ;各组 (除 组外 )分别结扎冠状动脉左心室支中点 ,缺血6 0 min,松开结扎线再灌注 2 4 0 min后 ( 组不进行再灌注 ) ,分别取结扎前、再灌注前、再灌注 2 4 0 min血测定内皮素 (endochelin ,ET)、一氧化氮 (nitric oxide NO)浓度和组织型纤溶酶原激活剂 (tissue- type plasminogen activa-tor,t- PA )、纤溶酶原激活剂抑制物 (,plasm inogen activator inhibitor PAI)活性。结果　冠状动脉结扎后 ,血浆ET、NO浓度和 PAI活性显著升高 (P<0 .0 1) ,t- PA活性显著下降 (P<0 .0 1) ,再灌注后 ,血浆 ET、NO浓度和 PAI活性进一步升高 ,t- PA活性进一步下降 ,与再灌注前对比均有显著性差异 (P<0 .0 1)。再灌注后 ,与 IR组对比 ,卡托普利、缬沙坦均能显著的升高 t- PA活性 ,降低血 PAI活性和 ET、NO浓度 (P<0 .0 1)。结论　卡托普利、缬沙坦有改善缺血再灌注过程中纤溶活性、抑制内皮细胞释放 ET、NO的有益作用     

银杏叶提取物对冠心病患者的氧自由基一氧化氮及纤溶活性的影响

目的研究冠心病病人血浆氧自由基与一氧化氮（NO）及纤溶活性的关系及银杏叶提取物的抗损伤作用。方法观察30例正常人及92例冠心病（稳定性心绞痛、不稳定性心绞痛、陈旧性心肌梗塞）病人血浆丙二醛（MDA）、超氧化物歧化酶（SOD）、NO、组织纤溶酶原激活物（t－PA）、t－PA抑制物（PAI）变化；并观察66例冠心病病人口服银杏叶提取物（天保宁）15天后上述指标的改变。结果三组冠心病人血浆MDA、PAI均显著高于正常人，SOD、t－PA、NO均显著低于正常人。病人服天保宁15天后可明显减少血浆中MDA、PAI，升高SOD、t－PA、NO水平。结论冠心病病人血浆氧自由基较正常人明显增高，并可引起血管内皮细胞损伤，NO合成减少，纤溶活性下降；而天保宁具有抗氧化损伤作用，增加NO合成，改善纤溶功能。     

脑梗塞早期患者血纤溶系统活性状态分析

为明确血纤溶系统活性状态与脑梗塞发病的关系，采用病例对照研究方法，对３０例皮质动脉区脑梗塞（ＣＡＣＩ）患者、３２例穿通动脉区脑梗塞（ＰＡＣＩ）患者及３０名无心脑血管病等的对照者，以发色底物分解产色法测定血浆组织型纤溶酶原激活物（ｔＰＡ）活性、纤溶酶原激活物抑制物（ＰＡＩ）活性及血管内皮ｔＰＡ释放能力和ＰＡＩ／ｔＰＡ比值，以综合判定其血纤溶系统活性，结果表明两种类型脑梗塞患者发病３天内血纤溶系统活性均显著低于对照者，为脑梗塞早期行溶栓治疗提供了理论依据。同时提出，再次脑梗塞可能与血浆ＰＡＩ活性高有关。     

冠心病介入治疗前后患者血浆P-选择素、血栓调节蛋白、纤溶酶原激活剂抑制剂-1的变化

目的旨在了解冠心病患者行经皮冠状动脉成形术(PTCA)前后血小板、内皮功能及纤溶活性的变化.方法以26例冠状动脉造影(CAG)阴性者为阴性对照,以16例CAG阳性但不宜行PTCA者为阳性对照,观察24例行PTCA术冠心病患者术前后P-选择素(Ps)、血栓调节蛋白(TM)及血浆纤溶酶原激活剂抑制物-1(PAI-1)的动态变化.结果PTCA组Ps、TM在术后5分钟较术前显著增加(P均<0.05),且较同时间点的阴性组有非常显著增高(P均<0.001);术后5minCAG阳性组Ps较CAG阴性组显著增加(P<0.02);在术前PTCA组和CAG阳性组PAI-1均高于CAG阴性组(P均<0.05).结论PTCA术后Ps、TM的增高,提示血小板的激活及内皮细胞的损伤,急性冠脉闭塞与PTCA后再狭窄可能与此相关.