尿激酶免疫脂质体靶向溶栓治疗兔肺动脉血栓栓塞

目的 观察以抗纤维蛋白D-二聚体单克隆抗体(DDmAb)为靶向装置的血栓靶向尿激酶(urokinase,UK)免疫脂质体(liposome,Lip)的溶栓效果.方法 新西兰大白兔32只,随机分为4组,每组8只,每只兔均采用自体血栓栓子颈静脉注入法建立急性肺动脉血栓栓塞模型.各组经股静脉输入不同溶栓剂进行溶栓治疗,通过观察右心室压变化及比较肺内残留栓子评价各组溶栓疗效.4组分别为阴性对照组(输入TBS缓冲液),阳性对照组(输入15万IU/kg UK),UK-Lip组(输入3万IU/kg尿激酶脂质体,反相蒸发法制备),DDmAb-UK-Lip组(输入3万IU/kg尿激酶免疫脂质体,戊二醛交联法连接UK-Lip和DDmAb制备).结果 栓塞后各组右心室压均明显升高(P均<0.01),平均升高(6.75±6.82)mm Hg(1 mm Hg=0.133 kPa).阴性对照组溶栓结束时右心室压[(40.15±11.22)mm Hg]与溶栓即刻[(41.67±14.23)mm Hg]相比下降轻微,阳性对照组和DDmAb-UK-Lip组降到与正常近似[阳性对照组和DDmAb-UK-Lip组溶栓结束时与栓塞前右心室压分别为(34.71±8.67)mm Hg比(33.98±9.32)mm Hg和(30.65±6.67)mm Hg比(30.77±6.85)mm Hg,P均>0.05],UK-Lip组情况居于阴性对照组和阳性对照组及DDmAb-UK-Lip组之间.阳性对照组及DDmAb-UK-Lip组栓子溶解最充分,残留柃子数近似(P>0.05),UK-Lip组栓子部分溶解,阴性对照组栓子未溶解.阳件对照组的心、肝、肾组织明显出血,其他组内脏未见明显病理学改变.结论 DDmAb-UK-Lip治疗急性肺动脉血栓栓塞的尿激酶用量仪为单独应用尿激酶的1/5即达到相似的溶栓效果,且不良反应较少,以DDmAb-UK-Lip进行靶向溶栓可能是肺动脉血栓栓塞的一种理想溶栓方式.     

超早期尿激酶溶栓治疗脑梗死的临床研究

目的评价超早期应用尿激酶(UK)2.0万U/kg溶栓治疗脑梗死的临床疗效及安全性。方法采用国产UK 2.0万U/kg静脉滴注,对66例发病6h内的脑梗死患者进行溶栓治疗,比较治疗前后神经功能缺损评分(NFDI)。另设60例普通治疗病人作为对照组。结果溶栓后2h NFDI为21.39±2.81,较溶栓前25.96±3.29明显减少(P<0.001),治疗后21d溶栓组NFDI为19.01±3.35,明显低于对照组22.67±3.68(P<0.001)。治疗后21d溶栓组的治愈率、显效率、总有效率分别为30.3%、66.7%、83.3%显著高于对照组13.3%、30%、46.7%,两组比较有显著性差异(均P<0.01)。结论在严格掌握溶栓治疗适应证基础上,应用国产UK 2.0万U/kg超早期静脉溶栓治疗脑梗死临床疗效好,并发症少。     

尿激酶静脉溶栓治疗急性脑梗死

目的评价尿激酶（UK）对6小时内急性脑梗死的疗效及其安全性。方法符合溶栓标准的病人236例随机分为溶栓组和非溶栓组。溶栓组120例,首先予尿激酶70万U,再予常规治疗14日。非溶栓组116例,只予常规治疗。应用中国脑卒中临床神经功能缺损程度评分标准进行评估神经功能恢复。结果溶栓组神经功能缺损评分迅速减少。溶栓组和非溶组在治疗后1日、15日、30日总有效率分别70%、85%、90%和20%、72%、83%,经Ridit分析,P〈0.05,具有非常显著性差异。颅内非症状性出血率3%（溶栓组）,2%（非溶栓组）;脑实质出血率3%（溶栓组）,0（非溶栓组）。结论UK用于治疗6小时内急性脑梗死有效且相对安全。     

尿激酶静脉溶栓治疗6小时内急性脑梗死

目的　评价尿激酶 (UK)对 6小时内急性脑梗死的疗效及其安全性。　方法　符合溶栓标准的病人118例随机分为溶栓组和非溶栓组。溶栓组 6 0例 ,首先予尿激酶 70万U ,再予常规治疗 14日。非溶栓组 5 8例 ,只予常规治疗。应用中国脑卒中临床神经功能缺损程度评分标准进行评估神经功能恢复。　结果　溶栓组神经功能缺损评分迅速减少。溶栓组和非溶栓组在治疗后 1日、15日、30日总有效率分别为 70 %、85 %、90 %和 2 0 %、72 %、83% ,经Ridit分析 ,P <0 0 1或P <0 0 5 ,具有非常显著性差异。颅内非症状性出血率 3% (溶栓组 ) ,2 % (非溶栓组 ) ;脑实质出血率 3% (溶栓组 ) ,0 (非溶栓组 )。　结论　UK用于治疗 6小时内急性脑梗死有效且相对安全。     

动静脉联合溶栓治疗急性缺血性卒中的临床研究

目的探讨动静脉联合溶栓治疗急性缺血性卒中的临床疗效及安全性。方法将65例发病在6h内的急性缺血性卒中患者随机分为两组:超选择性动脉溶栓 静脉溶栓组(联合组)共35例;超选择性动脉溶栓组(动脉组),30例。动脉组用微导管超选择病变动脉,尿激酶用量50万~150万U。联合组先静脉滴注尿激酶0.5万~1.0万U/kg,再动脉给尿激酶,总量不超过150万U。术前及术后6h、24h、7d、30d、90d采用欧洲卒中量表(ESS)评价神经功能缺损情况。结果治疗24h、30d后ESS评分联合组为83±24、88±26;动脉组为77±29、81±24。治疗后总再通率:联合组为42.8%,动脉组为33.3%,两组比较差异有显著性(P<0.05)。结论起病6h内,动静脉联合溶栓与动脉溶栓治疗相比,总再通率增加。     

短程小剂量尿激酶治疗急性心肌梗塞的疗效观察

近年来,国内外颇多文献报告溶栓治疗急性心肌梗塞(AMI)。我院1988年以来,对11例AMI患者采用短程小剂量尿激酶(UK)溶栓治疗,取得较好效果,而且无出血并发症。临床资料溶栓组11例,对照组14例,均系1988～1990年入院,发病在6小时以内,查无出血性疾病的AMI病人。溶栓组男10例,女1例,平均年龄56.9±8.7岁。对照组男6例,女8例,平均年龄62.07±6.2岁。溶栓方法采用0.9％生理盐水20ml+UK4万U,5分钟内静注后,续点0.9％生理盐水250ml+UK12万 U,2～4ml/min滴入。20分钟后再以0.9％生理盐水20ml+UK4万U静注1～2次,总量16～24万U,总疗程1～2小时。其他治疗措施同对照组,如吸氧、镇痛、扩冠、极化镁液静滴、阿     

用放射性血栓肺血栓栓塞症动物模型研究不同尿激酶溶栓方案的效果

目的　比较治疗肺血栓栓塞症 (PTE)时尿激酶 (UK) 2h和 12h溶栓方案的溶栓效果及特点。方法　 17只犬随机分为对照组 5只、UK 2h溶栓组 (UK2h组 ) 6只及UK 12h溶栓组 (UK12h组 ) 6只。利用新鲜放射性血栓PTE模型对两种UK溶栓方案进行对比研究。模型的溶栓率用核医学的感兴趣区技术 (ROI)及离体测定两种方法计算。结果　观察 14h ,利用ROI技术测定的对照组、UK2h组、UK12h组的溶栓率分别为 (6 2± 4 0 ) %、(39 5± 13 9) %、(16 9± 8 9) % ,3组相比 ,UK2h组的溶栓效果明显优于对照组及UK12h组 (P <0 0 1) ,而对照组与UK12h组之间差异无显著性 (P >0 0 5 ) ;UK2h组在溶栓后 4h出现明显的溶栓高峰 ,而UK12h组呈较均匀的缓慢溶解。利用离体法测定的 3组溶栓率分别为 (6 0± 2 7) %、(42 8± 12 4 ) %、(17 7± 9 3) %。两种方法测定的溶栓率有很高的相关性 (r =0 981,P <0 0 1)。结论　对于新鲜血栓 ,尿激酶 2h投药方案较 12h方案的溶栓率高 ,溶栓高峰明显。本实验模型是观察溶栓效果的较好实验方法。     

大剂量尿激酶静脉溶栓治疗急性心肌梗塞28例临床观察

目的探讨大剂量尿激酶(UK)静脉溶栓治疗急性心肌梗死的疗效。方法采用大剂量静脉溶栓疗法,首剂150万U,以后每天50万U静脉点滴,4～7d,总计300万～450万U。结果冠脉再通率82.14%(23/28),再梗率14.29%(4/28),出血并发症10.71%(3/28),病死率10.71%。结论大剂量尿激酶静脉溶栓治疗AMI病人,可以提高相关血管的再通率,降低病死率;溶栓治疗年龄不限;尿激酶150万U是AMI溶栓治疗较适当剂量。     

猪胰弹力蛋白酶血管外消化法制作兔颈总动脉梭形动脉瘤

目的探讨使用颈总动脉外膜消化法制作兔颈总动脉梭形动脉瘤的可行性和有效性。方法将16只新西兰大白兔按随机数字表法分为两组。实验组12只,使用猪胰弹力蛋白酶80~400 U孵育消化右侧颈总动脉起始点远端2~4 cm段。造模后1周行静脉血管造影,测量颈总动脉梭形膨大的宽度;取梭形扩张血管行苏木素-伊红(HE)染色及扫描电镜观察血管病理学变化。对照组取4只新西兰大白兔,使用等渗盐水孵育颈总动脉,1周后采用同样方法观察颈总动脉管腔及内膜变化。结果实验组12只新西兰大白兔在颈总动脉外膜消化后,血管造影显示10只模型兔颈总动脉管腔呈梭形扩大,梭形动脉最宽处直径为(3.70±0.32)mm,2只出现颈总动脉闭塞,较对照组右侧颈总动脉血管直径[(1.80±0.16)mm]明显增粗(P0.01);HE染色显示实验组兔右侧颈总动脉消化段管腔增宽,外膜及中膜减少;扫描电镜显示实验组兔颈动脉内膜炎性损伤及血栓附着。结论使用猪胰弹力蛋白酶消化颈总动脉外膜可以使兔颈总动脉呈梭形扩张,并造成颈动脉内膜损伤。使用此方法能够有效制作出梭形动脉瘤模型,具有一定的可行性。     

急性肺血栓栓塞症不同溶栓治疗方案的临床观察

目的:评估急性肺血栓栓塞症(PTE)3种溶栓方案的疗效和安全性。方法:将62例溶栓治疗的PTE患者随机分成3组,尿激酶(UK)组、重组组织型纤溶酶原激活剂(rt-PA)组、半量rt-PA+半量UK组,均用2 h溶栓方案,观察各组的疗效及出血发生率。结果:总有效率3组之间差异无显著性,但半量rt-PA+半量UK组治愈及显效率为65%,明显高于UK组37%,3组均无严重出血,UK组轻度出血的发生率明显高于其他2组,但rt-PA组有2例再栓塞。结论:半量的rt-PA+半量UK 2h溶栓方案可增加疗效,防止再栓塞,减少出血发生率,且治疗费用明显低于单纯rt-PA组。     

纳豆激酶对正常大鼠凝血系统的影响

目的通过检测正常大鼠的凝血酶原时间(PT)、活化部分凝血活酶时间(APTT)及凝血酶时间(TT),观察纳豆激酶(NK)冻干粉(NK-1)肌肉注射和固体发酶纳豆粉(NK-2)给药方式的NK抗凝血作用。方法将80只SD大鼠随机分为空白对照组、肝素对照1组、肝素对照2组、阿司匹林对照组、NK-1注射低剂量组、NK-1注射中剂量组、、NK-1注射高剂量组[注射剂量依次为1.6万～25.9万U/(kg·d)],NK-2口服低剂量组、NK-2口服中剂量组、NK-2口服高剂量组[口服剂量依次为0.5万～7.5万U/(kg·d)],每组8只。给药后观察各组大鼠血浆APTT、TT和PT指标变化。结果与空白对照组比较,NK-1注射高剂量组、NK-2口服高剂量组和阿司匹林对照组PT明显延长(P<0.05,P<0.01);肝素对照1、2组、NK-1注射低、中、高剂量组、NK-2口服高、中剂量组和阿司匹林对照组APTT明显延长(P<0.05,P<0.01);肝素对照2组、NK-1注射高剂量组TT明显延长(P<0.01)。结论 NK-1在1.6万～25.9万U/(kg·d)剂量范围内注射给药,与NK-2在0.5万～7.5万U/(kg·d)剂量范围内口服给药,对正常大鼠均具有一定的抗凝血作用,且抗凝血作用随剂量的升高而增强。     

Preventive effects of batroxobin on experimental canine coronary thrombosis

The thrombolytic effects of urokinase (UK) and preventive effects of batroxobin, heparin, and aspirin on the recurrence of thrombosis in the coronary artery were studied in 118 anesthetized dogs with severe endothelial denudation and luminal stenosis of the coronary artery. Occlusive thrombi developed in 68 (58%) preparations (dogs), accompanied by a decrease of coronary blood flow and pressure, an electrocardiographic ST elevation, and epicardial cyanosis. An intravenous infusion of 20,000 IU/kg of UK reopened the occluded coronary artery in all 32 preparations with 1-h-old thrombi, in 6 (86%) of 7 preparations with 2-h-old thrombi, and in 5 (83%) of 6 preparations with 3-h-old thrombi. However, recanalization was not observed in preparations with thrombi more than 4-h-old. Occlusion recurred within 6 h after recanalization in 2 (18%) of 18 preparations pretreated with batroxobin (1-2 BU/kg) (p> .005 vs. control UK group), in 1 (14%) of 7 preparations administered a continuous infusion of 30 U/kg per h of heparin (p > .05 vs. control UK group), in 4 (57%) of 7 preparations pretreated with 2 mg/kg of aspirin, and in 7 (64%) of 11 preparations not pretreated (control UK group). Complete prevention was observed only in the group administered 2 BU/kg of batroxobin. Histologically, these thrombi closely simulated clinical arterial thrombi. Myocardial hemorrhage and contraction band necrosis were observed in the reperfused hearts. In conclusion, experimental canine coronary thrombi more than 4-h-old were resistant to thrombolytic therapy, and batroxobin and heparin were effective in the prevention of coronary reocclusion.     

Randomized Clinical Trial of Urokinase versus Heparin in Unstable Angina

The aim of this study was to evaluate the clinical effect of urokinase (UK) in unstable angina (UA). This study was a multicenter, single-blind, heparin-controlled, randomized clinical trial. Entry criteria was that effort angina was significantly aggravated within 96 hours and angina attack at rest within 24 hours. In addition to the control group, thrombolytic therapy was divided into two groups according to the dose of UK. The high-dose group was 18,000 IU/kg, and the total dose was no more than 1.5 million IU (no bolus of heparin in this dose). The low-dose group was 14,000 IU/kg, and the total dose was no more than 1 million IU. All patients were treated by aspirin 300 mg/day and heparin 3000 U IV bolus before thrombolytic therapy (except for the high-dose group), then subcutaneous heparin 7,500 U q12h. The primary endpoint for the comparison between the thrombolytic and control groups was death and AMI (cardiac event) within 30 days of enrollment. Five hundred and fifty-six patients with UA were selected, and 272 and 284 patients were enrolled in thrombolytic group and control groups, respectively. The 30-day incidence of cardiac events was a little higher, but not significantly, in the thrombolytic group than in the control group (7.0% vs. 5.3%, ns), but the rate for cardiac events was much lower in the low-dose UK group than in the high-dose UK group. The difference was significant (3.3% vs. 10.0%, P < 0.05). Even if the rate was also lower than in the control group, this difference was not significant (3.3% vs. 5.3%, P > 0.05). The time interval between enrollment and the AMIs was quite different in these two groups. The majority of AMIs (73.7%) occurred within 24 hours, including 37% of AMIs that occurred within 2 hours after the beginning of thrombolytic therapy in the UK group. However, only small number of AMIs (20%) occurred within 24 hours of enrollment in the control group. The increase in AMI risk on the first day of thrombolytic therapy in this study might be closely related to thrombolysis and to the lack of strong antithrombin therapy. The risk of AMI might be remarkably reduced by using low-dose UK in combination with antithrombin therapy before thrombolytic therapy.     

Thrombolytic therapy for femoral artery thrombosis after pediatric cardiac catheterization

Femoral artery thrombosis remains a well-known complication after cardiac catheterization. A study was undertaken to assess the efficacy of thrombolytic therapy for this complication. A total of 526 consecutive infants and children were prospectively evaluated after cardiac catheterization, and the medical charts of 42 patients who required femoral artery thrombectomy between 1975 and 1985 were reviewed. In the prospective study, patients were given a bolus injection of heparin, 150 U/kg, at the time the artery was entered. Patients with persistently absent or diminished pulse 2 hours after catheterization received a second bolus injection of 50 U/kg followed by an infusion of 20 U/kg/hr heparin for a maximum of 48 hours. If the affected leg pulse was absent or reduced and the systolic Doppler blood pressure was less than two thirds that of the unaffected leg, thrombolytic therapy was begun. In the 42 patients with surgical thrombectomy, there were no serious complications of surgery. Forty-five of the 526 patients (8.6%) had a decreased or absent pulse after catheterization. Of these 45 patients, 32 (71.1%) improved with systemic heparinization only. Thirteen patients (28.9%) had a persistently absent pedal pulse suggesting femoral artery thrombosis, despite continuous heparinization. Eleven patients were successfully treated with thrombolytic therapy and two required surgical thrombectomy. Intraarterial balloon dilatation procedures were performed in 8 of these 13 patients. Prothrombin time was prolonged (11.5 +/- 1.06 to 52.3 +/- 40.4 seconds; p less than 0.025) and fibrinogen levels were significantly reduced (2.25 +/- 0.79 to 1.52 +/- 0.52 gm/dl; p less than 0.01) during therapy. There were no serious complications, although four patients bled from the groin entry site.(ABSTRACT TRUNCATED AT 250 WORDS)     

The beneficial effect of lys-plasminogen upon the thrombolytic efficacy of urokinase in a dog model of peripheral arterial thrombosis.

The efficacy of thrombolytic therapy may be limited by local availability of plasminogen near a poorly perfused thrombus. The purpose of this study was to determine if the local (i.e., clot site) administration of 0.5 mg glu-plasminogen (glu-plg) or 0.5 mg lysplasminogen (lys-plg) could safely increase the thrombolytic efficacy of a 30-min intraarterial injection of 3,500 U kg-1 of two-chain urokinase plasminogen activator (UK) in a dog model of arterial thrombosis. Thrombolysis was measured by monitoring the continuous decrement of 125I-gamma emissions from a radiolabeled thrombus. Reflow was evaluated by a distally placed flowmeter and by direct visual examination. Forty-two dogs (mean weight 10.1 +/- 1.9 kg) were randomly sorted into six groups of 7 each. The dogs in each group were given either saline plus saline (group 1), saline plus UK (group 2), glu-plg plus saline (group 3), glu-plg plus UK (group 4), lys-plg plus saline (group 5), or lys-plg plus UK (group 6) by selective arterial catheterization 60 min after formation of an occlusive thrombus. Ninety minutes following drug administration, all groups which received UK (groups 2, 4, and 6) showed greater lysis (p less than 0.05) than the groups which received only saline or either glu- or lys-plg plus saline. Group 6, which received lys-plg plus UK, showed significantly greater lysis (34 +/- 4%) than both group 2 (23 +/- 2%), which received saline plus UK, and group 4 (19 +/- 3%), which received glu-plg plus UK (p less than 0.05). All dogs (7/7) in group 6 had reflow at 90 min whereas only 3/7 dogs had reflow in both groups 2 and 4.(ABSTRACT TRUNCATED AT 250 WORDS)     

不稳定性心绞痛尿激酶溶栓治疗的临床疗效——多中心随机对照研究

目的　对比尿激酶 (UK)与肝素在治疗不稳定性心绞痛 (UA)中的疗效。方法　采用单盲 ,有对照的完全随机化方法。UK溶栓组中按UK使用剂量分为高剂量组和低剂量组 ,后者在溶栓前增加静脉推注 3 0 0 0U肝素。研究以 3 0天病死率和急性心肌梗塞 (AMI)发生率为终点指标。结果　总共入选UA患者 5 3 4例 ,高剂量UK组 14 8例 ,低剂量UK组 113例 ,相应肝素作为对照组各为 15 5和 118例。在心脏事件 (死亡 AMI例数 )的发生率上 ,高剂量UK组高于肝素对照组 ( 10 1%与5 2 % ,P >0 0 5 ) ;而低剂量UK组低于肝素对照组 ( 3 5 %与 5 1% ,P >0 0 5 ) ,但均未达到统计学差异 ,而溶栓组间比较 ,低剂量UK组的心脏事件发生率明显低于高剂量UK组 ( 3 5 %与 10 1% ,P <0 0 5 ) ,并达到统计学显著性差异。在心脏事件的发生时间上 ,高剂量UK组心脏事件大多发生在溶栓治疗首日 ,其中发生在UK治疗的头 2个小时内占 4 6 7% ,而对照组大多数发生在入选治疗的 2 4小时后 ( 80 %与 12 5 % ,P <0 0 0 5 )。结论　高剂量UK组溶栓首日AMI发生率明显增加 ,提示该溶栓治疗方案不适于不稳定性心绞痛的治疗 ,降低UK剂量 ,溶栓前加强抗凝血酶治疗 ,虽可明显减少AMI的发生率 ,但是否优于对照组仍需进一步探讨。     

Suzuki分级及异常代偿血管与成人烟雾病脑出血及缺血的关系

目的进一步探讨成人烟雾病患者脑出血及脑缺血事件的发生机制。方法对86例经全脑血管造影证实的成人烟雾病患者[脑出血52例(104个大脑半球,脑出血组),脑缺血34例(68个大脑半球,脑缺血组)]的临床资料进行回顾性分析,对Suzuki分级、烟雾样血管的丰富程度分期及颅内小动脉扩张不同者的脑出血及脑缺血发生率进行χ2检验及Mann-Whitney U检验。结果①两组Suzuki分级无显著差异,Mann-Whitney U检验Z=0.656、P=0.512;Suzuki分级Ⅲ～Ⅳ级者脑出血率显著高于脑缺血率(P<0.05)。②两组颅底烟雾样异常血管丰富程度分期有显著差异,Mann-Whitney U检验Z=3.909、P=0.000;其中2～4期者脑出血率显著高于脑缺血率(P<0.05)。③两组扩张小动脉无显著差异,Mann-Whitney U检验Z=1.183,P=0.237;同种血管扩张者脑出血率显著高于脑缺血率(P<0.05)。结论成人烟雾病患者脑出血及缺血发生与Suzuki分级无显著相关;烟雾样血管的丰富程度升高及颅内主要小动脉扩张预示脑出血事件发生的可能性大。     

Coronary thrombolysis. Comparative effects of intracoronary administration of recombinant tissue plasminogen activator and urokinase.

We employed a canine model of coronary thrombosis, induced by injection of radioactive blood clot, via a catheter placed in the left anterior descending coronary artery, to compare effects of intracoronary administration of recombinant tissue plasminogen activator (rtPA) and urokinase (UK) on rate and extent of coronary thrombolysis. Two doses of UK, 15,000 U/kg (UK15) and 30,000 U/kg (UK30) and two doses of rtPA, 0.25 mg/kg (rtPA.25) and 0.75 mg/kg (rtPA.75) were given. Drugs were infused over 45 min. Compared with the other regimens, rate and extent of coronary thrombolysis were significantly increased with rtPA.75. Also, despite a much higher dose of UK, coronary thrombolysis was similar with UK30 and rtPA.25. Compared with UK15, rate and extent of coronary thrombolysis were increased with rtPA.25. These results indicate that intracoronary administration of rtPA is superior to intracoronary UK in inducing thrombolysis.     

低剂量重组组织型纤溶酶原激活剂与尿激酶联合溶栓治疗急性脑梗死

目的观察联合应用重组组织型纤溶酶原激活剂（rt—PA）和尿激酶治疗急性脑梗死的有效性和安全性。方法选择发病〈6h的急性脑梗死患者81例,分为联合溶栓组（20例）、单用rt—PA组（22例）、单用尿激酶组（18例）及对照组（21例）。联合溶栓组静脉给予rt—PA20mg,尿激酶30万-50万IU;单用rt—PA组静脉给予rt—PA0．9mg／kg;单用尿激酶组静脉给予尿激酶1万～2万IU／kg（体质量超过75kg者按75kg给药）,最大剂量150万IU;未溶栓病例为对照组。主要疗效指标是观察治疗前与发病后4周的神经功能缺损评分（NIHSS）变化,以溶栓后出血转化、24h内再梗死及死亡等作为安全指标。结果联合溶栓组、单用rt—PA组、单用尿激酶组及对照组的观察结果为：①NIHSS评分治疗前分别为18．1±3．6、17．9±3．6、18．0±3．4、17．3±4．0,治疗后分别为9．1±5．6、8．8±5．5、9．6±5．2、14．1±4．6,符组治疗前、后比较,差异均有统计学意义（P〈0．01）,3个溶栓组与对照组比较差异均有统计学意义（P〈0．01）;3个溶栓组比较,差异无统计学意义。②4组治疗后总有效率分别为85．0％（17／20）、86．4％（19／22）、83．3％（15／18）和42．9％（9／21）,与对照组比较差异有统计学意义（P〈0．05）;各溶栓组间比较,差异无统计学意义（P〉0．05）。③联合溶栓组溶栓后24h内再发脑梗死1例,出血转化1例;单用rt—PA组出血转化3例;单用尿激酶组再梗死1例,出血转化有2例,其中死亡1例。对照组再梗死1例,死亡1例。结论与单用rt—PA和单用尿激酶比较,联合低剂量rt-PA和尿激酶溶栓治疗急性脑梗死同样安全、有效,相对rt—PA价格便宜,值得推广应用。