急性脑梗死患者血浆组织型纤溶酶原激活物与抑制物活性的动态变化

目的观察急性脑梗死不同时期患者血浆纤溶活性的动态变化,探讨其变化在病情发展中的作用。方法采用发色底物显色法测定60例脑梗死患者急性期与恢复期和60例同期住院非心、脑血管疾病患者血浆组织型纤溶酶原激活物(tissue-plasminogenactivator,t-PA)、纤溶酶原激活抑制物(plasminogenactivatorinhibitor,PAI)活性。结果脑梗死急性期组与恢复期组和对照组相比,t-PA活性明显减低,PAI活性显著增高(P均<0.01)。恢复期组与对照组比较差异无显著性意义(P>0.05)。结论急性脑梗死患者纤溶平衡失调,故检测其血浆t-PA,PAI活性动态变化可作为脑梗死诊断与治疗的一个客观参考指标。     

慢性心力衰竭患者血浆组织型纤溶酶原激活物和纤溶酶原激活物抑制物-1含量变化及其临床意义

目的　研究慢性心力衰竭 (CHF)患者血浆组织型纤溶酶原激活物 (t PA)和纤溶酶原激活物抑制物 1(PAI 1)含量的变化及其临床意义。方法　用酶联免疫吸附法 (ELISA)检测 6 0例CHF患者 (CHF组 )和 2 0例健康体检者 (正常对照组 )血浆t PA及PAI 1抗原含量。结果　CHF组血浆t PA和PAI 1平均含量都明显高于对照组 (P<0 .0 1)。CHF患者血浆PAI 1含量增高随心功能恶化而愈加明显。结论　CHF患者纤溶功能明显下降 ,可用血浆t PA、PAI 1含量作为判断病情的参考指标之一。     

去卵巢大白鼠血浆组织型纤溶酶原激活物与其抑制物的变化

测定了去卵巢大白鼠血浆组织型纤溶酶原激活物(t-PA)与纤溶酶原激活物抑制物(PAI)水平。与对照组比较去卵巢组血浆t-PA无显著性差异(P>0.05)。对照组PAI为9.7±1.2AU/ml,去卵巢组PAI为7.8±1.9AU/ml,两组比较有显著差异(P<0.05)。去卵巢组血浆中PAI降低,可能与卵巢激素的减少有关。卵巢激素会促使PAI合成并释放增加,这可能是服用雌激素等避孕药者纤溶活性降低、血液呈高凝状态的重要机制之一。     

组织型纤溶酶原激活物及其抑制物与缺血性脑卒中…

本文介绍了组织型纤溶酶原激活物及其抑制物的来源，基本结构及在纤溶系统中的主要作用，并对其对与缺血发表离卒中的发生，发展和恢复的关系以及运动对其产生的影响进行了综述。     

康复训练对脑血栓形成患者血浆组织型纤溶酶原激活物及抑 …

以４０例亚急性期、恢复早期脑血栓形成偏瘫患者为研究对象，随机分成康复治疗组和对照组，观察分析康复训练后即刻及３周后纤溶活性的变化。２０例健康老年人作为正常对照组。结果为：康复治疗后即刻、康复后３周与康复前相比，组织型纤溶酶原激活物活性分别提高３０％和１２．６％，组织型纤溶酶原抑制与激活物比值降低，纤溶活性增高（Ｐ〈０．０１），并高于对照组（Ｐ〈０．０１）。康复训练可部分逆转脑血栓形成患者组织型纤溶     

组织型纤溶酶原激活物及纤溶酶原激活物抑制剂对系统性红斑狼疮的检测价值

<正>自身免疫介导并累及多个系统、临床表现起伏是系统性红斑狼疮(systemic lupus erythematosus,SLE)的显著特征,血液、造血系统受损较常见,其发病机制仍不十分清楚[1]。SLE可以引起全身多器官损害并常存在高凝状态,甚至发生血栓或     

隐匿性冠心病病人血浆组织型纤溶酶原激活物及其抑制物活性…

用底物显色法测定了２９例隐匿性冠心病病人的组织型纤溶酶原激活物和纤溶酶原激活物抑制物的活性水平，结果发现隐匿性冠心病病人的ｔ－ＰＡ，ＰＡＩ活性与对照组比较，差异无明显性（Ｐ〉０．０５），提示血液中ｔ－ＰＡ，ＰＡＩ的活性异常仅是冠心病病人的发病因素之一。     

脑梗死患者检测纤溶系统及血小板参数的意义

目的探讨纤溶酶原激活剂抑制物-1、组织型纤溶酶原激活物及血小板参数在脑梗死患者中的变化。方法对60例脑梗死患者及60例健康体检者进行血小板及其参数、纤溶酶原激活剂抑制物-1、组织型纤溶酶原激活物的测量。结果与对照组相比,脑梗死患者中血小板、组织型纤溶酶原激活物含量显著低于对照组（P〈0.05）,平均血小板容积及血小板体积分布宽度及纤溶酶原激活剂抑制物-1含量显著高于对照组（P〈0.05）。结论血小板参数及纤溶酶原激活剂抑制物-1、组织型纤溶酶原激活物在脑梗死患者中有显著性改变,提示脑梗死患者存在着血小板活化及纤溶活性减低的现象,凝血系统活性改变在脑梗死患者的病情发展中起着一定的作用。     

康复训练对脑血栓形成偏瘫患者功能恢复的影响

以４０例急性期，恢复早期脑血栓形成偏瘫患者为研究对象，随机分为康复组和对照组，康复组运用神经促通技术，循序进行康复训练，心理疏导和适度的ＡＤＬ训练，功能评定采用Ｌｉｎｄｍａｒｋ感觉运动功能评定表和ＢａｒｔｈｅｌＡＤＬ指数，结果为３周后，康复组主动运动功能，快速运动变换能力，姿位转换及平衡功能明显提高，与康复前及对照组间差异显著；腕，手功能，行走能力与对照组无显著差异，ＡＤＬ指数提高，与对照组间存在     

高血压病患者血浆PAI-1、t-PA及t-PA/PAI-1水平的变化

目的通过对原发性高血压患者血浆纤溶酶原活化物抑制剂1(PAI-1)、组织型纤溶酶原活化物(t-PA)含量及t-PA/PAI-1比值的测定,了解高血压患者纤溶功能的情况。方法未用药物干预过的轻至中度原发性高血压患者(高血压组)64例,正常对照组42例,采用酶联免疫吸附双抗体夹心法测定两组血浆PAI-1、t-PA含量并计算t-PA/PAI-1。结果正常组PAI-1含量明显低于高血压组,(13.5±5.0)μg/L vs(53.0±22.6)μg/L(P<0.01);正常组t-PA/PAI-1明显高于高血压组,(0.83±0.52)μg/L vs(0.25±0.13)μg/L(P<0.01)。结论高血压患者的纤溶功能减退。     

不均匀恒磁场对小鼠血栓形成及血浆t—PA等的影响

目的研究不均匀恒磁场N极和S极对小鼠尾部血栓形成和血浆组织型纤溶酶原激活物(t-PA)及其抑制物(PAI)的影响.方法小鼠分组为空白对照组(A)、血栓对照组(B)、不均匀恒磁场N极组(C)和S极组(D),C、D组小鼠分别在N极朝向鼠体和S极朝向鼠体的鼠盒内饲养7d.用致血栓药角叉菜胶诱发小鼠体内血栓形成.发色底物法测定血浆t-PA及PAI活性.统计学处理用组间资料t检验.结果小鼠尾部平均血栓形成长度百分数C组和D组分别为(28.07±15.52)%和(21.37±16.50)%,比B组(43.73±17.25)%明显减少(依次为t=2.3102,0.01＜P＜0.05;t=3.2442,P＜0.01).C与D组间差异无显著性.B、C、D组与A组相比,t-PA活性明显下降(依次为t＝4.5037,P＜0.01;t＝2.5195,0.01＜P＜0.05;t＝2.3170,0.01＜P＜0.05).B、C组与A组相比,PAI活性明显增高(依次为t=5.1937,P<0.01;t=2.2340,0.01＜P＜0.05).C、D组与B组相比,PAI活性明显下降(依次为t=3.1663,P＜0.01;t=4.3874,P＜0.01).结论不均匀恒磁场有抗血栓作用.其作用机制可能与减少血浆PAI的释放有关.     

The safety and efficacy of repeated courses of tissue-type plasminogen activator in patients with stuck mitral valves who did not fully respond to the initial thrombolytic course

Summary.  In carefully selected patients with stuck mitral valves, thrombolytic therapy is becoming an established therapeutic modality. However, the management of patient with a suboptimal response to an initial thrombolytic course is unclear. The objective was to evaluate the efficacy and safety of re-administration of tissue-type plasminogen activator (rt-PA) in patients with stuck mitral valves in whom the first thrombolytic course has failed to restore normal prosthetic valve function. The study group included patients who received rt-PA and did achieve a full restoration of valve function after the initial course. Data were gathered on the safety and success rates of additional thrombolytic courses in the same hospitalization period, and their predictors. Twelve patients with stuck mitral valves experienced a total of 13 episodes in which a full resolution of leaflet abnormality was not achieved after the initial thrombolytic course. A repeated thrombolytic course was attempted in 10 patients (11 episodes). Six patients (60%) showed full success rate with repeated thrombolysis, one (10%) showed partial success, and three patients (30%) had no improvement following the second course. These last three were those with initial failure. Age, gender, valve model, worst functional class, time since valve implantation and International Normalized Ratio (INR) levels were similar in both groups. No major adverse events were noted.
In this small group of patients with stuck mitral valves, re-administration of rt-PA after a partial response to an initial thrombolytic course was effective and safe. However, total failure of the first thrombolytic course predicted inefficiency of further courses.     

Influence of thrombin-activatable fibrinolysis inhibitor and plasminogen activator inhibitor-1 gene polymorphisms on tissue-type plasminogen activator-induced recanalization in ischemic stroke patients

OBJECTIVE: Endogenous resistance to tissue-type plasminogen activator (t-PA) might decrease the benefit of thrombolysis-induced recanalization. Thrombin-activatable fibrinolysis inhibitor (TAFI) and plasminogen activator inhibitor-1 (PAI-1) are fibrinolysis inhibitors. TAFI removes residues from partially degraded fibrin that in turn eliminates plasminogen binding sites; PAI-1 directly inhibits the activity of t-PA. We aimed to study whether the presence of two common functional polymorphisms of the TAFI and PAI-1 genes influence rates of recanalization of the middle cerebral artery (MCA) among t-PA-treated stroke patients. METHODS AND RESULTS: TAFI and PAI-1 polymorphism determinations were performed by restriction fragment length polymorphism mapping and conventional sequencing in 139 patients with strokes involving the MCA and who received t-PA within 3 h. Recanalization was diagnosed by means of transcranial Doppler. No association was found between PAI-1 4 G/5 G polymorphism and recanalization rate. Dyslipidemia and TAFI Thr325Ile polymorphism were the main variables associated with recanalization resistance by the end of t-PA infusion: odds ratio (OR) 4.1 [95% confidence interval (95% CI) 1.6-10.8, P = 0.003] and OR 5.6 (95% CI 1.2-20, P = 0.031), respectively. The combination of the two polymorphisms doubled the risk of absence of recanalization: OR 11.1 (95% CI 1.4-89.8, P = 0.025). CONCLUSIONS: Polymorphic fibrinolysis inhibitor genes influence t-PA-induced recanalization resistance in ischemic stroke patients, especially when coexisting in the same patient. Efforts to individualize thrombolytic treatments are required.     

Antibodies to tissue-type plasminogen activator (t-PA) in patients with inflammatory bowel disease: high prevalence, interactions with functional domains of t-PA and possible implications in thrombosis

BACKGROUND: Patients with inflammatory bowel disease (IBD) have an increased prevalence of thromboembolic events. The pathogenetic mechanisms of these events include reduced fibrinolysis, which may be caused by antibodies to tissue-type plasminogen activator (t-PA). OBJECTIVES: To evaluate anti-t-PA antibodies in patients with IBD, considering clinical, biochemical and functional characteristics. PATIENTS AND METHODS: We immunoenzymatically measured anti-t-PA antibodies in plasma from 97 consecutive IBD patients and 97 age- and sex-matched healthy controls. We also assessed the antibody interactions with different epitopes of t-PA, the antibody inhibition on t-PA activity and the correlations with clinical features and other serum antibodies. RESULTS: IBD patients had higher median anti-t-PA antibody levels (5.4 U mL(-1) vs. 4.0 U mL(-1); P < 0.0001): 18 patients were above the 95th percentile of the controls (OR 5.3; 95% CI 1.7-16.3; P < 0.003), and the six with a history of thrombosis tended to have high levels (6.9 U mL(-1)). Anti-t-PA antibody levels did not correlate with IBD type, activity, location or treatment, or with age, sex, acute-phase reactants or other antibodies. The anti-t-PA antibodies were frequently IgG1 and bound t-PA in fluid phase; they recognized the catalytic domain in 10 patients and the kringle-2 domain in six. The IgG fraction from the three patients with the highest anti-t-PA levels slightly reduced t-PA activity in vitro. CONCLUSIONS: The prevalence of anti-t-PA antibodies is high in IBD patients. By binding the catalytic or kringle-2 domains of t-PA, these antibodies could lead to hypofibrinolysis and contribute to the prothrombotic state of IBD.     

纤溶酶原激活物抑制剂-1的研究进展

纤溶酶原激活物抑制剂-1(plasminogen activator inhibitor 1,PAI-1)作为体内组织型纤溶酶原激活物(tissue-type plasminogen activator,t-PA)和尿激酶型纤溶酶原激活物(urokinase-type plasminogen activator,u-PA)的主要抑制剂,与动静脉血栓、出血和凝血异常、细胞迁移密切相关,进而引起缺血性脑卒中、冠心病、静脉血栓、肿瘤转移、出血、股骨头坏死、流产等一系列疾病的发生发展。同时,体内血浆PAI-1活性水平又受血脂、血糖等调节,进一步参与肥胖、糖尿病、高脂血症等疾病的进程,又影响着上述相关疾病的预后。     

Fibrinolytic shut-down after surgery: impairment of the balance between tissue-type plasminogen activator and its specific inhibitor

In nine patients with non-malignant diseases undergoing major upper abdominal surgery, the mechanism of the postoperative fibrinolytic shut-down was investigated because of its potential significance for postoperative deep vein thrombosis by employing new and specific methods for assessing and stimulating the fibrinolytic system. The shut-down was found to result from an impairment of the balance between tissue-type plasminogen activator, t-PA, and its recently discovered fast-acting inhibitor. In this balance, the t-PA antigen concentrations both in resting conditions and after stimulation evoked by desamino-D-arginine vasopressin (DDAVP) were found to be unchanged by surgery. However, there was a significant postoperative increase in t-PA inhibitor levels. The release of t-PA under the stimulus of DDAVP infusion overcame the postoperative shut-down of t-PA activity. However, DDAVP infusion was associated with potentially unfavourable increases in the Factor VIII/von Willebrand factor complex. The discovery of increased t-PA inhibitor in the postoperative period opens new possibilities for a rational approach to reduce or abolish the postoperative fibrinolytic shut-down.