Subcellular distribution of urokinase and urokinase receptor in human neutrophils determined by immunoelectron microscopy

A high-affinity receptor for urokinase-type plasminogen activator (uPAR) has been identified on the plasmamembrane of a number of different cell types, and has been shown to be important for plasminogen activation, cell adhesion, and possibly signal transduction. uPAR and uPA cosediment with secretory vesicles and specific granules by subcellular fractionation and translocate to the plasma membrane upon activation of neutrophils. Here the subcellular distribution of uPAR and uPA is studied by electron microscopy of neutrophils using immunogold double labeling for uPAR and uPA and a set of markers for well-defined subtypes of granules: matrix metalloproteinase type-9 (MMP-9) for gelatinase granules, lactoferrin (LF) for specific granules, and myeloperoxidase (MPO) and neutrophil elastase (NE) for primary granules. With this technique uPAR colocalizes with uPA in 71% of labeled granules. In granules containing uPAR the degree of coexpression with MMP-9, MPO and NE was 19, 66, and 74%, respectively. In granules labeled for uPA the corresponding overlap with MMP-9, MPO and NE was 24, 64, and 51%, respectively. Low levels of co-localization were found for uPAR and LF (7%) and for uPA and lactoferrin (5%). The results indicate that uPAR and uPA arepresent in gelatinase granules and primary granules, but rarely in specific granules. The demonstration of uPAR and uPA in primary granules is of particular interest, and may indicate that uPAR and uPA participate in the activation of latent hepatocyte growth factor of neutrophils.     

经颅超声治疗联合静脉应用尿激酶改善急性脑梗死的预后

目的评估经颅超声治疗联合静脉应用尿激酶对急性缺血性卒中的疗效。方法单中心、前瞻性、随机对照临床研究。发病6h内的急性大脑中动脉缺血性卒中静脉应用尿激酶溶栓,随机分为800 kHz经颅超声治疗组和对照组,观察24 h内的早期症状改善和3个月时预后。结果与对照组相比,治疗组患者在24 h时症状明显改善(P0.05);3个月后,治疗组预后好(P0.05)。结论低频脉冲超声治疗联合静脉应用尿激酶明显改善了急性缺血性卒中的预后,且不增加颅内出血风险。     

血压对大鼠脑缺血/再灌注损伤的影响

目的： 研究血压变化对大鼠脑缺血/再灌注模型的影响。方法: 44只SD大鼠随机分为低血压组、正常血压组、高血压组及尿激酶/高血压组,制作缺血2 h再灌注24 h脑缺血/再灌注损伤模型,再灌注起始分别应用降压药物或升压药物改变平均动脉压水平（约20 mmHg）持续1 h,观察其神经功能改善、梗死体积、出血性转化的发生。结果: 再灌注24 h,低血压组神经功能恶化,其它各组均有不同程度的恢复;随着血压的升高,大鼠脑梗死体积有逐渐减小的趋势;尿激酶/高血压组出血性转化发生率最高,其次为低血压组及高血压组,而正常血压组最低;尿激酶/高血压组梗死灶周围皮层区MMP-9阳性细胞计数与其它各组比较均有显著差异（P<0.05）。结论: 再灌注期间升高血压有利于脑缺血大鼠神经功能预后的改善。大鼠脑缺血再灌注模型出血性转化发生率随着血压的升高或降低均有增加的趋势,其发生可能与MMP-9的过量表达有关。     

小剂量尿激酶治疗具有溶栓相对禁忌证的肺栓塞患者的临床观察

目的探讨小剂量尿激酶溶栓治疗对具有溶栓相对禁忌证的急性肺栓塞患者的疗效及安全性。方法将具有溶栓相对禁忌证、病情危重的39例肺栓塞患者,每日1次用小剂量尿激酶（50万IU）2h溶栓治疗,连用3～7d。同时监测血凝,每次于溶后2h根据APTT值开始肝素抗凝。观察其疗效及并发症。结果溶栓过程中均未见有大出血。39例中,死亡6例（3例死于顽固性低氧血症,3例死于原发病）,其余33例患者症状明显改善。结论具有溶栓相对禁忌证的肺栓塞患者,用小剂量尿激酶溶栓治疗,具有良好的临床疗效及安全性。     

包裹性结核性胸膜炎的临床治疗观察

目的观察胸腔内注射尿激酶治疗包裹性结核性胸膜炎的可行性和安全性。方法对照组30例予以2HRZE/4HRE抗结核方案,B超定位下胸膜腔穿刺抽液,并口服强的松激素。观察组在对照组基础上在每次胸穿抽液后胸腔内注射尿激酶10万单位(用20ml生理盐水稀释)。结果观察组和对照组总有效率分别为96.8%和63.3%,观察组疗效明显优于常规对照组,差异有显著性(P<0.05)。观察组和对照组抽液次数比较,无显著性差异(P>0.05),但两组抽液量、积液吸收时间、胸膜粘连及胸膜厚度比较,差异有显著性(P<0.05)。观察组所有患者均对尿激酶治疗耐受良好,无出血倾向等严重的不良反应。结论胸腔内注入尿激酶治疗包裹性结核性胸膜炎可增加引流量,减轻胸膜肥厚,改善肺功能,减轻患者痛苦,疗效显著。     

早期尿激酶静脉溶栓治疗急性心肌梗死51例临床观察

目的观察早期尿激酶静脉溶栓治疗急性心肌梗死的临床疗效及不良反应。方法回顾性分析笔者所在医院102例心肌梗死患者的临床资料,51例采用早期尿激酶静脉溶栓术治疗,另51例采用常规治疗,观察两组患者的再通情况。结果采用尿激酶静脉溶栓治疗组的冠脉再通率为68．6％,对照组为11．8％,两组比较差异有显著性意义（P〈0．05）。结论早期使用尿激酶静脉溶栓术治疗急性心肌梗死能提高疗效,降低病死率。     

尿激酶溶栓后即刻PCI与直接PCI治疗STEMI的比较

目的:比较溶栓后即刻经皮冠状动脉介入治疗(即刻PCI)与直接PCI治疗急性ST段抬高心肌梗死(STEMI)的安全性和疗效。方法:分析接受PCI治疗的连续130例STEMI患者冠脉病变及干预情况,随机分为尿激酶150万单位溶栓后即刻PCI和直接PCI两组,记录术中慢血流无血流、出血并发症、平均住院日、院内死亡率及平均18.1个月随访期间终点事件发生率。结果:两组临床特征及冠状动脉病变相似(P>0.05),即刻PCI组与直接PCI组相比,就诊-球囊时间、术中无血流慢血流、PCI成功率、出血并发症、平均住院日、院内死亡率以及18.1个月心血管事件发生事均无显著差异(P均>0.05)。结论:即刻PCI不增加出血并发症,但近期疗效和远期预后并未发现优于直接PCI。     

小剂量尿激酶治疗急性脑梗塞的TCD临床研究

目的:观察小剂量尿激酶对治疗急性脑梗塞前后的经颅多普勒(TCD)改变.方法:在小剂量尿激酶治疗的前中后分3次观察TCD前后对照.结果:治疗前与治疗后有显著意义.结论:TCD对溶栓治疗效果评定及急性脑梗塞预后判断有重要意义.     

尿激酶胸膜腔注入治疗结核性包裹性胸腔积液临床观察

目的 观察胸膜腔内注入尿激酶治疗包裹性结核性胸膜炎的效果。方法 对28例结核性胸膜炎于抽液后注入尿激酶10-25万IU并观察效果。结果 治疗组中治愈18例，有效8例，无效2例，和对照组相比（治愈3例，有效10例，无效7例），差异有统计学意义（P〈0．05）。结论 胸膜腔内注入尿激酶可有效溶解纤堆，促进胸水吸收。是治疗结核性包裹性胸膜炎的有效方法。     

Thrombolytic therapy with tissue plasminogen activator for the treatment of nonstructural malfunction of bileaflet cardiac valve prostheses

This study was conducted to determine the effect of thrombolytic therapy with tissue plasminogen activator (t-PA) for nonstructural malfunction of bileaflet cardiac valve prostheses. Twenty-seven patients with bileaflet prosthetic valve malfunction diagnosed by a combination of cineradiography and transthoracic echocardiography were treated with the administration of intravenous t-PA. The treatment resulted in complete success in 55.6% (15 of 27), partial success in 22.2% (6 of 27), and no change in 22.2% (6 of 27). In the complete success and partial success groups, the condition of the patients in 85.7% (18 of 21) of the cases improved within 24 h after the administration of t-PA. Six cases in whom thrombolytic therapy was instituted more than 1 month (ranged from 1 to 38 months, mean 14.7 months) after the diagnosis of prosthetic valve malfunction showed significantly less effectiveness of thrombolytic therapy with t-PA. Only one patient (3.7%) had a major complication (thromboembolism) after t-PA treatment. The results suggest that thrombolytic therapy with t-PA in patients with nonstructural malfunction of bileaflet cardiac valve prostheses is effective with low incidence of complication when the treatment is instituted early after the diagnosis.