缺血性脑血管病纤溶活性和血清同型半胱氨酸含量测定的临床意义

目的　探讨缺血性脑血管病 (ICVD)患者血浆纤溶活性和血清同型半胱氨酸 (Hcy)含量的变化及其临床意义。方法　入选ICVD患者 86例 (ICVD组 ) ,根据病情又分为短暂脑缺血发作 (TIA)组 14例 ,脑梗死组 72例 ,并入选非脑血管病患者 4 3例作为对照组 ,分别采用产色法测定血浆纤溶酶原 (Plg)、组织型纤溶酶原激活物 (t PA)、纤溶酶原激活抑制物 1(PAI 1)活性 ,荧光偏振光法测定血清Hcy,电化学发光法测定叶酸 ,同时常规测定血脂水平。结果　ICVD组 ,TIA患者和脑梗死患者血浆Plg、t PA活性均较对照组显著降低 (P <0 .0 5 )。ICVD组血清Hcy水平较对照组明显升高 (P <0 .0 1) ,t PA活性降低和高Hcy对ICVD的发生均有显著作用。结论　t PA活性降低和高Hcy分别是ICVD的独立危险因素     

缺血性心脑血管疾病患者血浆纤溶酶原激活物及纤溶酶原激活物抑制剂1的测定及临床意义

目的研究缺血性心脑血管疾病患者血浆尿激酶型纤溶酶原激活物及其受体、组织型纤溶酶原激活物及其抑制剂1的水平及意义。方法应用酶联免疫吸附试验测定急性脑梗死、急性心肌梗死及不稳定型心绞痛患者血浆尿激酶型纤溶酶原激活物及其受体、组织型纤溶酶原激活物及其抑制剂1的水平。结果(1)脑梗死患者急性期血浆尿激酶型纤溶酶原激活物轻度升高(P>0.05),恢复期明显回落(P<0.05),尿激酶型纤溶酶原激活物受体水平在急性期明显升高(P<0.01),恢复期进一步升高;血浆中组织型纤溶酶原激活物含量在急性期明显低于对照组(P<0.01),而纤溶酶原激活物抑制剂1含量则明显高于对照组(P<0.01),恢复期纤溶酶原激活物抑制剂1水平趋于正常,而血浆中组织型纤溶酶原激活物水平与对照组比较仍存在一定差异(P<0.05)。(2)急性心肌梗塞患者血浆尿激酶型纤溶酶原激活物受体水平急性期明显升高(P<0.05),恢复期进一步升高(P<0.01),尿激酶型纤溶酶原激活物水平均大致正常;急性期血浆中血浆中组织型纤溶酶原激活物及纤溶酶原激活物抑制剂1含量均明显高于对照组(P<0.01),恢复期明显回落,纤溶酶原激活物抑制剂1趋于正常,血浆中组织型纤溶酶原激活物水平仍高于对照组(P<0.05)。(3)不稳定型心绞痛患者急性期(入院时)血浆尿激酶型纤溶酶原激活物受体水平明显升高(P<0.01),恢复期(入院后二周)回落,但仍明显高于对照组(P<0.05),尿激酶型纤溶酶原激活物水平与对照组比较均未见明显差异(P>0.05);急性期血浆中组织型纤溶酶原激活物含量明显低于正常组(P<0.01),而纤溶酶原激活物抑制剂1含量略高于对照组(P>0.05),恢复期两者含量均趋于正常(P>0.05)。结论缺血性心脑血管疾病患者存在不同程度的凝血纤溶系统失平衡,对疾病的发生发展起重要作用。     

脑梗死患者血浆纤溶指标的动态观察

目的　探讨脑梗死患者血浆中纤溶分子标志物———组织纤维蛋白溶酶原激活剂 (TPA)和纤溶酶原激活物抑制剂 (PAI 1)含量的动态变化及其临床意义。方法　采用酶免疫定量法对 30例首次急性脑梗死患者急性期和恢复期的血浆TPA和PAI 1含量进行测定 ,并选择 30名正常人作为对照。同时对比首次急性脑梗死 30例和再发脑梗死 2 8例急性期血浆TPA及PAI 1含量。结果　首次急性脑梗死患者恢复期的TPA低于急性期 ,高于正常对照组 ;PAI 1含量脑梗死恢复期明显高于急性期。再次发病急性脑梗死患者比首次发病急性脑梗死患者的PAI 1高。结论　PAI 1与脑梗死的发生与发展有着重要关系 ,应作为临床的重要危险因素对待。     

降压药物治疗对纤溶功能的影响

组织型纤溶酶原激活物 (t PA)及其抑制剂 1(PAI 1)的动态平衡决定了纤溶功能 ,高血压患者多存在纤溶功能减低 ,临床常用的六类降压药物对血浆t PA和PAI 1水平有着不同的影响。     

脑血栓患者t-PA与PAI的测定及临床意义

我们采用发色底物显色法测定了24例脑血栓急性期与恢复期患者的组织型纤溶酶原激活剂(t-PA)与纤溶酶原激活剂抑制物PAI的活性,并与15例正常人对照,以探讨脑血栓时t—PA与PAI的变化及其临床意义。     

凝血纤溶指标的变化与缺血性心脏病的关系

为探讨缺血性心脏病（IHD）患者的凝血、纤溶变化及其临床意义，用高效液相色谱仪测定了26例急性心肌梗塞（AMI）、26例不稳定型心绞痛（UAP）、20例正常对照者的尿纤维蛋白肽A（FPA）、并用相应方法同步测定了血浆D－二聚体（D－Dimer）、组织型纤溶酶原激活物（t－PA）及其抑制物（PAI）活性、并对其中UAP患者进行跟踪随访。结果表明：AMI、UAP患者尿FPA值均比对照组高；血浆D－Dimer水平及PAI活性亦高，t－PA活性降低，且AMI和UAP患者之间也有显著性差异。经随访发现半年内发展为AMI的UAP者当初其尿FPA值和血浆D－Dimer值均较高。表明凝血纤溶系统的变化在IHD的发生、发展中起着重要作用、研究凝血纤溶指标对于探讨其发病机理及预后判定均有一定帮助。     

肾病综合征患者纤溶酶原激活物及其抑制物的变化及低分子肝素干预研究

肾小球硬化的病理生理基础是肾小球细胞外基质(ECM)积聚 ,纤溶酶原激活物及其抑制物 (PA/PAI)是调节ECM降解的重要酶系 ,研究表明肾炎病变组织中存在PA/PAI的异常表达[1] ,但在肾炎患者血浆中的变化报道甚少。本研究测定原发性肾病综合征 (NS)患者血浆组织型纤溶酶原激活物 (tPA)、尿激酶型纤溶酶原激活物 (uPA)、尿激酶型纤溶酶原激活物受体 (uPAR)、纤溶酶原激活物抑制物 1(PAI 1)的改变以及低分子肝素 (LMWH)干预治疗对上述指标的影响。1　对象和方法1.1　研究对象　选择本院 2 0 0 1- 0 4～ 2 0 0 3- 0 5确诊的原发性NS …     

脑卒中急性期凝血系统和纤溶系统变化的临床意义

20 0 2年 1月至 2 0 0 2年 12月 ,我们对 114例脑卒中急性期患者进行了血浆凝血系统、纤溶系统检测。现报告如下。临床资料 :患者组共 114例 ,男 6 5例 ,女 4 9例 ;年龄 4 2～ 85岁 ,平均 6 1.5岁 ;均为脑卒中急性期。对照组 6 0例 ,男 34例 ,女2 6例 ;年龄 5 2～ 77岁 ,平均 5 9.5岁 ;均为同期体检健康者。患者组入院后次日晨空腹采静脉血 ,对照组早晨空腹采静脉血 ,用3.2 %枸橼酸钠 0 .2 m l+静脉血 1.8ml抗凝混匀 ,迅速分离血浆进行检测。蛋白 C(PC)、组织型纤溶酶原激活物 (t- PA)、组织型纤溶酶原激活物抑制物 (PAI)检测采用发色底…     

短暂脑缺血发作患者急性期凝血-纤溶活性异常的研究

目的 探讨短暂脑缺血发作（TIA）的患者急性发作期是否存在凝血纤溶系统异常,并判断其与预后的相关性.方法 检测随机选取的50例急性期（＜3 d）的TIA患者的凝血-纤溶指标的活性,根据简单的“6分-ABCD”评分标准将TIA患者分为：高危组（ABCD评分≥5分,18例）和低危组（ABCD评分＜5分,32例）,并与50例正常对照组比较.结果 （1）TIA各组血清假性血友病因子（vWF）、纤维蛋白肽A（FPA）、D-二聚体（D-dimer）水平、纤溶酶原激活物抑制物（PAI）活性均高于对照组,组织型纤溶原激活物（t-PA）活性明显低于对照组（P＜0.01）.（2）TIA患者高危组的vWF、FPA水平和PAI活性亦高于低危组（P＜0.05）,而D-dimer、t-PA并无显著性差异.结论 （1）TIA患者急性期存在血管内皮的损伤、血液高凝状态及微血栓的形成,其血浆vWF、FPA、t-PA、PAI、D-dimer在一定程度上反映了凝血功能变化.（2）vWF、FPA水平和PAI活性的测定有助于早期判断患者的预后,为临床干预提供依据.     

脑梗死急性期和恢复期血管内皮细胞和纤溶功能的变化

观察脑梗死急性期患者和恢复期患者的血管内皮细胞和纤溶功能的变化。应用酶标法、免疫扩散法和发色底物法对82例脑梗死急性期患者和124例脑梗死恢复期患者进行血液学观察并与92例正常人对照。结果发现，与对照组比较，脑梗死急性期患者的血管性假血友病因子明显升高。6-酮-前列腺素Flα和组织型纤溶酶原激活物活性明显下降：脑梗死恢复期患者的纤溶酶原、组织型纤溶酶原激活物抗原和组织型纤溶酶原激活物活性明显下降，脑梗死急性期和恢复期患者的纤溶酶原激活物抑制剂均轻度升高。脑梗死恢复期患者的血管性假血友病因子、纤溶酶原、组织型纤溶酶原激活物抗原和组织型纤溶酶原激活物活性较脑梗死急性期患者明显下降，但均未恢复正常。结果提示，脑梗死急性期患者和恢复期患者都存在明显的血管内皮细胞和纤溶功能异常，临床上不仅要重视脑梗死急性期的治疗，对恢复期患者仍要积极治疗。     

Changes in coagulation and tissue plasminogen activator after the treatment of cerebral infarction with lumbrokinase

This paper aimed to investigate the effect of lumbrokinase on the anticoagulation and fibrinolysis in treating cerebral infarction. Lumbrokinase was used in patients with cerebral infarction. Patients were randomly divided into treatment group (n = 31) and control group (n = 20). Single blind method was used in this investigation. The Chinese stroke score was used to evaluate the results of treatment before and after administration of lumbrokinase. Kaolin partial thromboplastin time (KPTT), prothrombin time (PT), fibrinogen content, vWF content were analyzed, and tissue plasminogen activator (t-PA) activity, plasminogen activator inhibitor (PAI) activity, D-dimer level were assayed. In both groups, the stroke score decreased after administration, but in the treatment group, it was more obvious. In the treatment group, KPTT was prolonged, t-PA activity and D-dimer level increased, while the content of fibrinogen decreased significantly. There were no significant changes of PT and PAI activity in both groups. It is concluded that lumbrokinase is beneficial to the treatment of cerebral infarction. The effect of lumbrokinase is related to the inhibition of intrinsic coagulation pathway and the activation of fibrinolysis via an increase of t-PA activity.     

疏血通注射液对高卒中风险短暂性脑缺血发作患者纤溶系统及预后的影响

目的探讨疏血通注射液对高卒中风险的短暂性脑缺血发作(transient ischemic attack,TIA)患者凝血-纤溶系统及短期预后的影响。方法 70例ABCD2评分6分～7分TIA患者随机分为两组。所有患者均接受标准的综合治疗,治疗组加用疏血通注射液。所有患者诊断后24h内行凝血酶原时间(PT)、活化部分凝血酶原时间(APTT)、纤维蛋白原(Fg)、D-二聚体(DD)及组织型纤溶酶原激活物(t-PA)和纤溶酶原激活物抑制剂(PAI)浓度测定,在入院后3d、5d、7d、10d重复测定上述指标。随访时间为3个月。主要转归指标为急性脑梗死和死亡。结果两组患者基线均存在t-PA下降及Fg、PAI水平增高。治疗组患者Fg水平于第5天下降,PAI浓度于第7天下降;对照组观察期内Fg、PAI浓度无显著差异。治疗组短期转归明显优于对照组(P<0.05)。结论疏血通注射液治疗能有效降低Fg和PAI水平,改善高卒中风险的TIA患者近期转归。     

The pathogenesis of accelerated fibrinolysis in hepatosplenic schistosomiasis.

Seventy patients with different stages of hepatosplenic schistosomiasis and 18 non-bilharzial normal controls were studied. Plasminogen, plasminogen activators (PA), tissue-type plasminogen activator (t-PA), urokinase-type plasminogen activator (u-PA), alpha 2-antiplasmin (alpha 2-AP), plasminogen activator inhibitor (PAI), fibrinogen/fibrin degradation products (FDP) and D-dimer were determined to elucidate the role of plasminogen activators and inhibitors in the pathogenesis of accelerated fibrinolysis in schistosomiasis. There was a progressive increase in the levels of PA, t-PA, u-PA, FDP and D-dimer indicating enhanced fibrinolytic activity with advancing disease. In addition, there was progressive decrease of plasminogen, alpha 2-AP and PAI levels which might be due to decreased hepatic synthesis and/or increased peripheral consumption. These findings suggest that the pathogenesis of accelerated fibrinolysis in schistosomiasis is multifactorial, but may be due to the progressive increase in the levels of plasminogen activators. In addition, the increase of FDP and D-dimer levels are evidence of secondary fibrinolysis following thrombin generation.     

高血压及合并急性脑梗死患者血浆同型半胱氨酸与组织型纤溶酶原激活物及其抑制剂的关系

为研究高血压及高血压合并急性缺血性脑血管病中高同型半胱氨酸水平对凝血、纤溶系统的影响。用高效液相色谱法分别测定21例健康人、28例单纯高血压患者及30例高血压合并急性脑梗死患者血浆同型半胱氨酸水平，同时测定纤维蛋白原、组织型纤溶酶原激活物和组织型纤溶酶原激活物抑制剂，分析三组患者上述指标的关系。结果发现，高血压及合并急性脑梗死组同型半胱氨酸、组织型纤溶酶原激活物、组织型纤溶酶原激活物抑制剂及纤维蛋白原均高于健康对照组，高血压合并急性脑梗死组同型半胱氨酸、组织型纤溶酶原激活物抑制剂及纤维蛋白原均高于高血压组，而组织型纤溶酶原激活物低于高血压组。结果提示，高血压及合并急性脑梗死患者存在血浆同型半胱氨酸水平增高，且高同型半胱氨酸浓度可能引起纤溶、凝血功能的紊乱，并在脑梗死的发病中起一定作用。     

Impaired fibrinolysis in coronary artery disease

We assessed endogenous endothelial-dependent fibrinolysis in 99 subjects with coronary artery disease (CAD) documented by angiography and in 28 control subjects with normal coronary arteries on angiography. We used specific, sensitive assays for plasma tissue-type plasminogen activator (t-PA) antigen, t-PA activity, plasminogen activator inhibitor (PAI) activity, plasminogen, and alpha-2 plasmin inhibitor (alpha-2 PI). Mean PAI activity was significantly higher, and mean t-PA activity after venous occlusion of the upper arm (a standard test of the capacity of vascular endothelium to release t-PA) was significantly lower in subjects with CAD than in subjects with normal coronary arteries. The mean increment in t-PA antigen after venous occlusion was significantly lower than normal in subjects with CAD with onset of symptoms before age 45 years. Subjects with CAD had a significantly increased mean plasma fibrinogen level compared with control subjects, and a significant positive correlation was observed between PAI activity and plasma fibrinogen in subjects with CAD. No significant abnormalities of plasminogen or alpha-2 PI were observed in any subset of subjects with CAD. These data support an association between impaired fibrinolysis and CAD, with contributions from both increased PAI activity and in younger subjects from reduced endothelial t-PA release.     

老年高血压并发脑梗死患者凝血、抗凝、纤溶系统功能改变及意义

目的分析老年高血压并发脑梗死患者凝血、抗凝、纤溶系统分子标志物指标的变化及意义，为临床早期诊断治疗提供客观依据。方法检测100例老年高血压患者、100例老年高血压合并脑梗死患者及100例健康老年对照者血管性血友病因子抗原（vWF：Ag）、血小板α-颗粒膜蛋白-140（GMP-140）、纤维蛋白原（FIB）的含量及抗凝血酶（AT）、蛋白S（PS）、蛋白C（PC）、组织型纤溶酶原激活剂（t-PA）、纤溶酶原激活剂抑制物-1（PAI-1）的活性，并进行分析与评价。结果与对照组相比，老年高血压患者、老年高血压合并脑梗死患者血浆vWF：Ag、GMP-140、FIB含量、PAI-1活性均明显升高，而AT、PS、PC、t-PA活性明显降低，差异具有统计学意义（P〈0．01）。结论老年高血压患者存在明显的凝血、抗凝及纤溶功能失衡，这与其病情进展及脑梗死的发生密切相关，早期防治具有重要的临床意义。     

Interrelationship between coagulant activity and tissue-type plasminogen activator (t-PA) system in acute ischaemic heart disease. Possible role of the endothelium.

Patients with unstable angina pectoris (UAP; n = 20) and acute myocardial infarction (AMI; n = 34) were studied in the acute phase of ischaemic heart disease. We found significantly higher levels of thrombin-antithrombin-III (TAT) complexes, lower levels of systemic tissue plasminogen activator (t-PA) activity, and higher levels of plasminogen activator inhibitor (PAI) activity in the AMI patients compared to the UAP patients. In contrast to these specific changes, general acute phase reactants such as C-reactive protein, fibrinogen and von Willebrand factor did not differ significantly between the two groups. Studies of the relationship between coagulation (TAT-complexes) and fibrinolysis data revealed a significant positive correlation between plasma antigen concentrations of TAT-complexes and t-PA (P less than 0.02), and between TAT-complexes and PAI-I (P less than 0.002). These observations indicate a common pathophysiological mechanism underlying the changes in coagulation and fibrinolysis, suggesting that coagulation activity and t-PA-related fibrinolysis are interrelated processes in vivo, and probably take place at the level of the endothelial cell.     

无症状性脑梗死患者血清炎性因子和纤溶及抗纤溶活性的变化

目的观察无症状性脑梗死(silent cerebral infarction,SCI)患者血清炎性因子和纤溶及抗纤溶活性的变化。方法选择SCI患者53例(SCI组)和健康体检者55例(对照组),分别检测血清高敏C反应蛋白(hs-CRP)、血浆纤溶酶原活性(PLG:A)、纤溶酶活性(PLM:A)、组织型纤溶酶原激活物(t-PA)活性、D-二聚体(D-D)含量、_2α-纤溶酶抑制剂(α_2-PI)和纤溶酶原激活物抑制剂(PAI)活性。结果 SCI组hs-CRP水平明显高于对照组[(15.36±4.30)mg/L vs (10.26±2.61)mg/L,P<0.01],SCI组PLM:A、t-PA和D-D含量均明显低于对照组[(35.84±10.23)% vs (68.74±18.41)%,(0.11±0.01)U/ml vs (0.49±0.12)U/mL(0.36±0.14)mg/L vs (0.68±0.16)mg/L,P<0.01)],SCI组PLG:A与对照组比较差异无统计学意义(P>0.05),SCI组α_2-PI活性和PAI活性明显高于对照组[(128.46±23.75)% vs (96.36±19.34)%,(0.86±0.22)AU/ml vs (0.48±0.10)AU/ml.P<0.01]。结论炎症过程和纤溶及抗纤溶系统的功能失调与SCl的形成有关。     

Increased levels of fibrinolysis reaction products (D-dimer) in patients with decompensated alcoholic liver cirrhosis.

We studied the activation of coagulation and fibrinolysis in the blood of patients with compensated (n = 25) and decompensated (n = 25) liver cirrhosis. We observed increased blood concentrations of thrombin-antithrombin III (TAT) complexes (p less than 0.001) and of D-dimer (p less than 0.001) in both groups of patients compared with healthy volunteers (n = 25). The blood levels of tissue-type plasminogen activator (t-PA) activity (p less than 0.001) and the concentrations of t-PA antigen (p less than 0.001) were also significantly raised in both groups of patients compared with controls, whereas plasminogen activator inhibitor did not deviate. There were no significant differences in the determined variables between the two groups of patients except that the concentrations of D-dimer were significantly higher (p less than 0.001) in patients with decompensated liver cirrhosis. The ratio between D-dimer and TAT did not deviate between patients with compensated liver cirrhosis and healthy volunteers but was significantly increased in patients with decompensated liver cirrhosis. These observations indicate that efflux from the extravascular space (for example, ascitic fluid) contributes to the high concentrations of fibrin degradation products (D-dimer) in patients with decompensated liver cirrhosis. In addition, we conclude that patients with liver cirrhosis have an enhanced activation of both coagulation and fibrinolysis but that the balance between these two systems is not significantly displaced compared with healthy volunteers.