老年冠心病患者纤溶酶原激活抑制剂的变化

目的探讨老年人冠心病与纤溶酶原激活抑制剂（PAI）的关系。方法测定了93例老年冠心病患者的PAI和组织型纤溶酶原激活剂（t-PA）活性、胆固醇和甘油三酯的血浆水平,并与健康对照组比较。结果冠心病组的PAI活性〔（810±360）AU/L〕明显高于健康对照组〔（640±300）AU/L,P＜0.01〕;冠心病组的t-PA活性〔（390±140）IU/L〕明显低于对照组的水平〔（490±240）IU/L,P＜0.05〕。结论老年人PAI活性的增高和t-PA活性的降低可能参与了冠心病的发病机制。     

体外治疗性超声对大鼠纤溶系统的影响

目的　研究体外治疗性超声对大鼠血浆组织型纤溶酶原激活因子 (t-PA)、纤溶酶原激活物抑制因子 -1(PAI -1)的影响。方法　采用酶联免疫吸附法测定超声治疗前后大鼠血浆t-PA、PAI -1的改变。结果　超声治疗后ETUS组t-PA(0 .5 4± 0 .19)IU/ml,PAI -1(0 .44± 0 .18)AU/ml,对照组t -PA(0 .5 1± 0 .2 5 )IU/ml,PAI -1(0 .43± 0 .19)AU/ml,二者比较无明显差异 (P >0 .0 5 )。结论　治疗剂量超声对大鼠纤溶系统没有影响     

永久性心脏起搏对纤溶系统的影响

目的探讨不同模式永久性心脏起搏对纤溶系统的影响。方法随机选择安装永久性心脏起搏器患者54例,根据起搏模式分为两组,其中VVI起搏器36例(V组),DDD起搏器18例(D组)。选择32例起搏器术前患者作对照组(C组)。测定组织型纤溶酶原激活剂(t-PA)活性、a2-纤溶酶抑制剂(a2-PI)活性、纤溶酶原灭活剂(PAI)活性及D-二聚体(D-D)浓度。结果V组和D组的PAI活性明显高于C组(P<0.01),V组和D组之间差异也有统计学意义(P<0.05)。V组和D组的t-PA活性却明显低于C组(P<0.01),其中V组又低于D组(P<0.05)。PAI/t-PA比值的改变与PAI活性改变相似;PAI/t-PA比值与术后时间之间没有线性相关关系(P>0.05)。V组的a2-PI活性高于C组(P<0.05)。各组之间D-D浓度差异无统计学意义(P>0.05)。结论置入永久性心脏起搏器患者纤溶功能处于低下状态,尤其以单腔心室起搏为明显。     

运动负荷对不稳定性心绞痛患者纤溶活性影响的研究

对20例健康受试者和25例不稳定性心绞痛患者进行运动负荷前、后组织型纤溶酶原激活剂(t-PA)、纤溶酶原激活剂抑制剂(PAI-1)活性的测定.结果发现运动前静息时,两组t-PA活性无显著差异,而PAI-1活性不稳定性心绞痛组明显高于对照组;运动后,不稳定性心绞痛组t-PA活性显著低于对照组(0.96±0.45IU/ml对1.89±0.68IU/ml,P<0.01),PAI-1活性下降幅度小于对照组(12.0%对31.9%),使其PAI-1活性仍显著高于对照组(8.20±2.28AU/ml对4.21±0.68AU/ml,P<0.01).提示不稳定性心绞痛患者不论是静息,还是在运动负荷激发后,均存在着纤溶活性的下降.     

脑梗死患者血清脂蛋白(a)水平和纤溶系统活性的测定及相互关系

目的探讨脑梗死患者血清脂蛋白(a)水平、组织型纤溶酶原激活剂(t-PA)和纤溶酶原激活剂抑制物-1(PAI-1)活性的变化及它们之间的相互关系,研究脂蛋白(a)与缺血性脑血管病的关系。 方法 对137例急性脑梗死患者和54例健康者(对照组),采用速率散射比浊法检测血清脂蛋白(a)水平,发色底物法检测血浆t-PA与PAI-1活性,并进行比较。 结果脑梗死组血清脂蛋白(a)水平为(343±136)mg／L,血浆PAI-1活性为(896±97)AU／L,对照组血清脂蛋白(a)水平及PAI-1活性分别为(205±110)mg／L和(587±142)AU／L,两组比较差异有显著意义(P<0.01);脑梗死组t-PA活性为(223±77)IU／L,对照组为(424±121)IU/L,两组比较差异有显著意义(P<0.01)。脑梗死组血清脂蛋白(a)水平与t-PA活性呈显著负相关(r=-0.326,P<0.01),与PAI-1活性呈显著正相关(r=0.796,P<0.001)。结论脂蛋白(a)通过降低t-PA的活性和(或)增强PAI-1的活性,干扰纤溶系统的平衡,从而参与动脉粥样硬化过程。高脂蛋白(a)水平是缺血性脑血管病的重要独立危险因素。     

不稳定型心绞痛患者纤溶活性及内皮功能的变化

目的观察不稳定型心绞痛患者血浆组织型纤溶酶原激活物(t-PA)、纤溶酶原激活物抑制物-1(PAI-1)、假性血友病因子(vWF)水平的变化,进一步明确纤溶活性和内皮功能在不稳定型心绞痛中的作用,并探讨其临床意义。方法选择40例不稳定型心绞痛患者和30例健康志愿者,均取早晨空腹静脉血,用发色底物法测定血浆t-PA和PAI-1的活性,用酶联免疫吸附双抗体夹心法测其血浆中vWF的含量。结果(1)不稳定型心绞痛组的t-PA活性明显低于对照组(0.2±0.11IU/ml∶0.4±0.09IU/ml,P<0.05),而PAI-1活性则较对照组增高(0.9±0.32AU/ml∶0.53±0.30AU/ml,P<0.05),vWF含量较对照组明显增高［(565±80.5)%∶(80±55.6)%,P<0.001］;(2)PAI-1活性与vWF的含量呈正相关;(3)PAI-1活性、vWF含量均与甘油三酯水平呈正相关。结论纤溶活性降低、血管内皮受损使不稳定型心绞痛患者易发生冠状动脉痉挛及血栓形成。     

高原肺水肿患者血浆纤溶系统变化及卡托普利的影响

目的　观察高原肺水肿 (HAPE)患者血浆纤溶系统的变化及卡托普利对其的影响 ,探讨其发病机制。方法　 72例高原肺水肿患者分为卡托普利组 (35例 )和常规组 (37例 ) ,并以 2 0名健康志愿者作为对照。所有患者治疗前、后均测定血浆组织型纤溶酶原激活物 (tPA)及纤溶酶原激活物抑制物 (PAI 1)的活性。结果　血浆tPA含量卡托普利组 (A组 )治疗前、后分别为 (0 4 0± 0 14 )× 10 3 IU/L、(0 5 8± 0 13)× 10 3 IU/L ,常规组 (B组 )治疗前、后分别为 (0 39± 0 19)× 10 3 IU/L、(0 4 9± 0 16 )×10 3 IU/L ,正常对照组 (C组 )为 (0 5 9± 0 17)× 10 3 IU/L ;A、B两组治疗前、后比较差异均有显著性(P <0 0 1、<0 0 5 ) ;血浆PAI 1含量A组治疗前、后分别为 (6 6± 1 8)× 10 3 AU/L、(4 9± 1 5 )×10 3 AU/L ,B组治疗前、后分别为 (6 6± 1 6 )× 10 3 AU/L、(5 8± 1 7)× 10 3 AU/L ,C组为 (4 9± 1 3)×10 3 AU/L。A、B两组治疗前、后比较差异均有显著性 (P <0 0 1、 <0 0 5 )。结论　HAPE患者纤溶系统呈失衡性改变 ,卡托普利有恢复其平衡的治疗作用。     

凝血及纤溶系统变化在急性心肌梗塞溶栓治疗中的作用

本文通过对急性心肌梗塞(AMI)早期溶栓治疗的43例患者进行凝血及纤溶系统功能的测定,分别在溶栓前、溶栓后4h、12h、24h、48h及1周测定凝血酶原时间(PT)、活化的部分凝血活酶时间(APTT)、纤溶酶原(PLG)、α_2抗纤溶酶(α_2AP)、纤维蛋白原(Fg)、D二聚体含量(D=Dimer)、组织型纤维溶酶原活化物(t-PA)、组织型纤溶酶原活化物抑制物(PAI),其结果显示,溶栓组冠脉再通26例(60.5%),溶栓前与溶栓后4h相比冠脉再通组t-PA活性明显高于未通组(P<0.01),PLG活性及Fg含量的降低幅度再通组明显高于未通组,建议溶栓中应把测定t-PA、PAI、PLG及Fg作为判断溶栓治疗效果的指标.     

冬虫夏草对糖尿病大鼠纤溶系统的影响

目的 观察冬虫夏草 (CS) 对糖尿病肾病 (DN)大鼠纤溶系统功能的影响.方法 44只大鼠随机分为正常对照组、模型组 (给予链脲佐菌素55 mg/kg体重腹腔注射),CS早期干预组及冬虫夏草晚期干预组,12 w后测体重、肾重、血糖、血肌酐 (Scr)、24 h尿蛋白等指标,光镜观察肾脏病理变化,免疫组化法分别检测组织型纤溶酶原激活物 (t-PA)/纤溶酶原激活物抑制剂表达 (PAI).结果 模型组肾重、血糖、Scr、24 h尿蛋白均明显高于正常对照组(P＜0.01),PAI表达明显高于正常对照组,体重、t-PA表达明显低于正常对照组;两干预组肾重、Scr、血尿素氮 (BUN)、24 h尿蛋白、t-PA表达均高于模型组(P＜0.05),低于正常对照组(P＜0.01),体重、PAI表达低于模型组,高于正常组,血糖较模型组无明显变化;冬虫夏草早期干预组效果优于晚期干预组(P＜0.05).结论 DN时存在t-PA/PAI失衡,冬虫夏草治疗DN的机制之一为矫正t-PA/PAI失衡.     

尿激酶治疗下肢深静脉血栓的纤溶研究

35例下肢深静脉栓塞(lower legs deep venous thrombosis,LDVT)患者,应用尿激酶治疗,探讨治疗前后纤溶酶原活性(PLG:A),纤溶酶活性(pL:A),组织纤溶酶原激活物(t-PA),组织纤溶酶激活物抑制物(PAI)和纤维蛋白原抗原性(Fg:Ag)的变化,结果显示PAI和Fg:Ag明显降低(P值分别<0.05和<0.001),pl:A呈显著增高(P值<0.001)。同时,下肢深静脉栓塞部分与完全再通24例(24/35例),疗效达68.5%,无1例出血与过敏。由此证实尿激酶具有明显溶栓效应,且安全可靠。     

High PAI activity with correlation to triglyceride and HDL cholesterol values in patients with coronary artery disease with no difference in survivors of myocardial infarction

Summary The fibrinolytic capacity of blood depends mainly on the amount of tissue-type plasminogen activator (t-PA) activity and plasminogen activator inhibitor type-1 (PAI-1) activity. Previous studies linked high PAI activity or low t-PA activity with the development of atherosclerosis and thromboembolic diseases. Yet, there are conflicting reports in the literature as to whether there is higher PAI activity in patients with myocardial infarction (MI) than in patients with coronary artery disease (CAD) without previous MI. In this retrospective study, t-PA activity, t-PA antigen, and PAI activity before and after a venous occlusion test (VOT) of 10 min were assessed in 109 patients with angiographically documented CAD, in two subgroups of CAD patients with (n=66) or without (n=43) previous MI, and in subgroups of CAD patients according to their triglyceride levels and other risk factors. The mean values of t-PA activity in the whole patient group showed a 100-fold increase and a 3.1-fold increase in t-PA antigen after VOT (0.03±0.03 to 3.0±6.8 U/ml and 16.5±6.9 to 51.0±25.4 ng/ml,p<0.05). PAI activity was 24.4±11.0 before and 19.6±13.2 U/ml after VOT. Within the CAD group, no difference was found between patients without MI and survivors of previous MI in PAI activity before VOT (24.6±10.7 vs. 24.3±11.3 U/ml) and after VOT (19.0±12.1 vs 20.0±14.0 U/ml), or t-PA activity before (0.03±0.01 vs. 0.04±0.04 U/ml) and after VOT (2.8±7.0 vs. 3.2±6.7 U/ml). In 39.4% of CAD patients elevated plasma PAI activity before VOT (>25 U/ml) was found. This subgroup of patients represented the highest PAI activity after VOT (p<0.05), the lowest t-PA activity after VOT (p <0.001), and the highest triglyceride levels (p<0.05). In 11% of the patients, a small increase in t-PA activity (less than 0.5 U/ml) after VOT was seen. This group showed the lowest t-PA antigen after VOT (p<0.001) and the highest fibrinogen level (p<0.05). Both subgroups showed the same distribution among patients with and without MI. CAD patients with triglyceride levels over 200 mg/dl had the highest PAI activity values before VOT (28.3±11.8 U/ml;p<0.01) and after VOT (24.9±13.2 U/ml;p <0.01), resulting in low t-PA activity after VOT.(p<0.01). Additionally, a negative correlation was found between PAI activity and HDL cholesterol (p<0.001). No differences were found between subgroups of CAD patients separated according to smoking habits, blood pressure, cholesterol, and severity of CAD. This study confirms former findings of elevated PAI activity in patients with coronary artery disease. In contrast to some reports, it did not demonstrate a difference between patients with and without previous MI. Further studies may clarify whether changes in lipid metabolism influence the function of endothelial cells in synthesis or secretion of PAI. Prospective studies are necessary to determine whether high PAI activity is a risk factor for the development of coronary artery disease or MI.     

老年前列腺癌患者去势后性激素水平变化及对凝血和纤溶系统的影响

目的探讨老年前列腺癌患者去势后性激素水平变化及对血液凝血和纤溶系统活性的影响。方法27例早期前列腺癌经手术去势的患者作为研究组,39例非前列腺癌老年患者作为正常对照组。分别测定黄体生成素(LH)、卵泡刺激素(FSH)、总睾酮(TT)、游离睾酮(FT)、雌激素(E2)、部分凝血酶原时间(PT)、活化部分凝血酶时间(APTT)、纤维蛋白原(Fib)、凝血酶原活动度(PA)、纤溶酶原(PLG)活性、α2-抗纤溶酶(α2-PI)活性、抗凝血酶-Ⅲ(AT-Ⅲ)活性、二磷酸腺苷(ADP)活性、D-二聚体(DD)含量、血小板聚集率和黏附率、组织型纤溶酶原激活剂(t-PA)及组织型纤溶酶原激活剂抑制物(PAI-1)抗原浓度。结果研究组中患者TT、FT、E2水平显著降低,E2降低幅度小于TT,LH、FSH、FT/TT、E2/TT显著升高;PT、APTT显著缩短,Fib及DD含量显著增加,血小板聚集率、黏附率及ADP活性均显著升高,PLG、α2-PI活性显著增强,t-PA抗原含量及t-PA/PAI-1显著下降,PAI-1含量显著增加。AT-Ⅲ活性无显著变化。结论前列腺癌患者去势后性激素比例严重失调;血小板活性及血液凝血活性显著增强,纤溶活性显著抑制,提示去势患者存在发生动脉硬化的高度危险性。     

联合检测血浆D-二聚体、基质金属蛋白酶-9对急性主动脉夹层的诊断及预后判断价值

目的 研究联合检测血浆D-二聚体（plasma d-dimer,D-D）、基质金属蛋白酶-9（matrix metalloproteinase-9,MMP-9）对急性主动脉夹层的诊断及预后判断价值。方法 以2012年1月至2016年12月期间沧州市中心医院急诊科收治的急性主动脉夹层患者200例为研究对象,记为主动脉夹层组。另取同时期沧州市中心医院急诊科就诊的胸痛患者200例记为对照组。比较两组患者病历资料、病史、血压、血浆D-D、MMP-9水平。采用受试者工作特征曲线（receiver operating characteristic curve,ROC）判断血浆D-D、MMP-9单独检测以及联合检测诊断急性主动脉夹层的效能。对急性主动脉夹层组患者随访12个月,其中死亡组31例、生存组169例。结果急性主动脉夹层组收缩压[(165.32±14.83)mm Hg比(112.57±11.76)mm Hg,t=39.415]与舒张压[(97.82±9.74)mm Hg比(86.39±8.25)mm Hg,t=16.342]分别高于对照组,差异均有统计学意义（P均<0.05）。急性主动脉夹层组患者血浆D-D[(1.62±0.84)mg/L比(0.37±0.19)mg/L,t=20.526]与MMP-9[(1327.32±398.57)ug/L比(256.38±89.74)ug/L,t=37.071]水平分别高于对照组,差异有统计学意义（P均<0.05）。D-D联合MMP-9诊断急性主动脉夹层的敏感度为0.807、特异度为0.815。急性主动脉夹层死亡组患者血浆D-D[(2.43±1.02)mg/L比(1.41±0.77)mg/L,t=6.423]与MMP-9[(1745.73±414.92)ug/L比(1105.67±346.17)ug/L,t=9.165]水平分别高于生存组,差异有统计学意义（P均<0.05）。结论 联合检测血浆D-D、MMP-9应用于急性主动脉夹层中的诊断效能较高,可能成为患者预后评估的有效指标。     

纤维蛋白原对内皮细胞t-PA和PAI-1 mRNA表达的影响

目的 探讨纤维蛋白原（Ｆｇ）对内皮细胞（ＥＣ）组织型纤溶酶原激活物（ｔ－ＰＡ）和纤溶酶原灭活剂（ＰＡＩ－１） ｍＲＮＡ表达的影响。方法 不同浓度Ｆｇ与ＥＣ孵育不同时间后,用单管逆转录聚合酶链反应（ＲＴ－ＰＣＲ）半定量法检测ｔ－ＰＡ和ＰＡＩ－ｍＲＮＡ的表达。结果 用２０,２００,２０００ｍｇ／Ｌ Ｆｇ与ＥＣ孵育１、１２、２４ｈ、ＰＡＩ－１ ｍＲＮＡ的相对表达水平分别为同时相对照组的１．７,３．６,２     

肺血栓栓塞症患者凝血纤溶系统及肺血管内皮功能的变化

目的探讨肺血栓栓塞症(PTE)患者体内凝血纤溶系统及肺血管内皮功能的变化及其临床意义。方法采用酶联免疫吸附测定(ELISA)检测80例PTE患者(急性大面积PTE组20例、非大面积PTE组60例)、40名正常人(对照组)的血D-二聚体(D-D)、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)、血浆蛋白S(Ps)、血浆蛋白C(Pc)、凝血酶调节蛋白(TM)、抗心磷脂抗体(ACA)、同型半胱氨酸(Hcy)含量;采用发色底物法检测抗凝血酶Ⅲ活性(AT-Ⅲ)。结果急性大面积PTE组患者血D-D、t-PA、PAI-1、Ps、TM、含量分别为(1.46±0.62)mg/L、(11.4±6.9)μg/L、(88.2±27.5)μg/L、(22.40±9.40)mg/L、(6.8±1.1)μg/L,非大面积PTE组分别是(0.92±0.27)mg/L、(6.6±1.5)μg/L、(60.1±26.1)μg/L、(23.90±10.70)mg/L、(6.3±1.5)μg/L,均显著高于正常对照组的(0.38±0.10)mg/L、(4.7±1.4)μg/L、(35.7±9.2)μg/L、(16.10±6.20)mg/L、(3.0±0.5)μg/L(分别P<0.01、<0.05)。急性大面积PTE组患者血AT-Ⅲ含量为(86.0±11.8)%,非大面积PTE组为(90.1±9.0)%,显著低于正常对照组的(102.6±9.20)%(P分别<0.01、0.05)。两PET组患者ACA-IgG、IgM、IgA显著高于正常对照组,差异有统计学意义(P<0.05)。结论PTE患者存在凝血纤溶系统功能失衡和肺血管内皮损伤。     

伊拉地平对高血症病患者血小板功能和纤溶活性的影响

本文测定了１２例高血压病患者经伊拉地平（Ｉｓｒａｄｉｐｉｎｅ）（１．２５ｍｇ～２．５ｍｇ，１日２次）治疗８周前后和１０例健康对照者的血小板聚集性（ＰＡｇ）、血浆组织型纤溶酶原激活剂（ｔ－ＰＡ）及其抑制物（ＰＡＩ）活性。结果表明，高血压组ＰＡｇ、ＰＡＩ活性明显高于对照组，ｔ－ｐＡ活性显著低于对照组；伊拉地平治疗后，ＰＡｇ、ＰＡＩ活性显著降低，ｔ－ＰＡ活性显著升高。本文提示：高血压病患者存在血小板功能亢进和纤溶活性降低，伊拉地平能够抑制血小板聚集，增强纤溶活性，在防治心脑血管并发症方面具有重要意义。     

The dynamic changes of plasma tissue-type plasminogen activator level and the activity of its inhibitor during coronary vasospasm

This study aimed to examine the dynamic changes of the fibrinolytic system during coronary vasospasm. Tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor (PAI) and fibrinopeptide A (FPA) levels were measured in the great cardiac venous and arterial blood of 9 patients with clinically and angiographically proven vasospastic angina and 11 controls. Before ergonovine provocation, although there was no difference between the above 2 groups in t-PA levels in the aorta or the great cardiac vein, the PAI level in patients with variant angina was lower than in the controls both in the aorta (4.2 +/- 3.5 IU/ml vs 10.9 +/- 5.2 IU/ml) and in the great cardiac vein (2.3 +/- 2.9 IU/ml vs. 11.9 +/- 4.9 IU/ml). During ergonovine-induced coronary vasospasm in patients with variant angina, the t-PA level in the great cardiac vein significantly increased from 3.4 +/- 0.7 ng/ml to 4.4 +/- 0.5 ng/ml (p less than 0.05), but it did not change in the aorta. The maximal dose of ergonovine (0.4 mg) induced mild diffuse coronary vasoconstriction in the controls, and this diffuse coronary vasoconstriction induced a reduction of PAI levels in the great cardiac vein from 11.9 +/- 4.9 IU/ml to 9.5 +/- 4.8 IU/ml (p less than 0.05). FPA levels in the great cardiac vein did not change during ergonovine-induced coronary vasospasm in either group. Thus, the coronary vasospasm induced the release of t-PA from endothelial cells of coronary vessels and resulted in the reduction in the PAI activity in the great cardiac vein.(ABSTRACT TRUNCATED AT 250 WORDS)     

Endothelial Tissue-Type Plasminogen Activator Release in Coronary Heart Disease: Transient Reduction in Endothelial Fibrinolytic Reserve in Patients With Unstable Angina Pectoris or Acute Myocardial Infarction

Objectives. We sought to examine whether the disturbed fibrinolytic system in patients with an acute coronary syndrome is associated with a reduced endothelial fibrinolytic capacity.Background. Intracoronary thrombus formation is a frequent finding in acute coronary syndromes. Systemic alterations of coagulation and fibrinolysis are known to occur, but possible disturbances of endothelial fibrinolytic function have not been investigated.Methods. We compared 42 patients with an acute coronary syndrome (acute myocardial infarction in 11 and unstable angina pectoris in 31) with 25 patients with stable angina. Venous blood was sampled serially for determination of markers of the fibrinolytic system and of hypercoagulability from admission to day 10. An occlusion test to determine the maximal endothelial tissue-type plasminogen activator (t-PA) release was also performed.Results. Both on day 0 and day 10, patients with an acute coronary syndrome had a marked elevation of t-PA mass concentration (mean value ± SEM 14.4 ± 1.6 [day 0], 18.9 ± 2.5 ng/ml [day 10]) and of plasminogen activator inhibitor (PAI) (9.4 ± 2.2 [day 0], 11.3 ± 2.6 AU/liter [day 10], p < 0.05 vs. patients with stable angina). There was also a hypercoagulative state with elevated thrombin activity and increased D-dimers (p < 0.05 vs. patients with stable angina). Maximal endothelial t-PA release was initially reduced (p < 0.05 vs. patients with stable angina) to 2.3 ± 0.9 ng/ml, but levels recovered during follow-up to 4.4 ± 1.4 ng/ml (vs. 5.7 ± 1.5 ng/ml in patients with stable angina).Conclusions. Despite the known prolonged systemic alteration of fibrinolysis in acute coronary syndromes, endothelial fibrinolytic capacity is reduced only during the acute phase and becomes normalized during follow-up, and thus is linked more to intravascular thrombus formation than to steady state levels of markers of the fibrinolytic system.