Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.73 (urokinase-type plasminogen activator)
 10,685 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The levels of tissue-type plasminogen activator (t-PA), plasminogen activator inhibitor (PAI) and other substances of coagulation-fibrinolysis, such as fibronectin (Fn) and von willebrand factor (vWF) as well as the activity content of antithrombin-III(AT-III) in plasma were determined in 20 patients with acute myocardial infarction (AMI). In 11 of them these measurements were carried out before and after the treatment with urokinase (UK1000 000 IU). The results suggested that the function of coagulation-fibrinolytic system was disturbed in AMI. Thrombolytic treatment with UK could interfere and improve the stabilization of fibrinolytic activity in the body, but these actions last only short time. Some substances of coagulation showed change with UK treatment.
Zhonghua Nei Ke Za Zhi 1991 Apr
PMID:[The kinetics of plasma coagulation fibrinolysis levels in acute myocardial infarction before and after treatment with intravenous urokinase]. 190 71

Twenty cases of primary nephrotic syndrome were treated with urokinase at a dosage of 60,000 units per day for two successive weeks. The results showed that after treatment the concentrations of fibrinogen, urine FDP, alpha 2-plasma inhibitor and plasminogen were significantly decreased (P value less than 0.01, less than 0.01, less than 0.001, less than 0.005 respectively). The concentration of antithrombin III was significantly increased (P less than 0.05). It is suggested that the treatment obviously increased the fibrinolytic activity and improved the hypercoagulated state. The clinical data showed that in addition to decrease of proteinuria and obvious increase of urine volume, the clinical manifestations and laboratory parameters showed no significant difference. Further study on the dosage and indications of urokinase is needed and the activity of coagulation and fibrinolysis in patients with deep vein thrombosis of lower extremities was also discussed.
Zhonghua Nei Ke Za Zhi 1989 Jun
PMID:[Primary nephrotic syndrome treated with urokinase--a report of 20 cases]. 258 15

The degree of platelet activation and damage in 15 cases with acute myocardial infarction (AMI) receiving thrombolytic therapy and 15 cases with AMI receiving anticoagulant therapy were studied in vivo and in vitro by using specific monoclonal antibodies (SZ-51 & S12) against alpha-granule membrane protein 140 (GMP-140). Clinical indexes and myocardial enzyme changes in the two groups of patients were also observed. The results showed that the number of GMP-140 molecules on platelet surface and the concentration of GMP-140 in plasma were increased before treatment. The number of GMP-140 molecules on platelet surface began to decrease on the 1st day and returned to baseline on the 7th day after treatment. The concentration of GMP-140 in plasma reached a peak on the 1st day, began to fall on the 2nd day and returned to baseline on the 3rd day after treatment. There were no significant differences in the dynamic changes of number of GMP-140 molecules on platelet surface and the concentration of GMP-140 in plasma between groups of thrombolytic therapy and anticoagulant therapy. In vitro experiment showed that the thrombolytic medicine urokinase neither activated platelets nor inhibited platelet activation induced by thrombin. Significantly greater reperfusion rate and earlier appearance of CK and CK-MB peaks were found in the thrombolytic than in the anticoagulant group. LVEF determined by echocardiography, rate of return of ST segments to baseline and alleviation rate of chest pain were significantly greater and complications of AMI (ventricular fibrillation, left ventricular failure and angina) were less in the group receiving thrombolytic therapy.(ABSTRACT TRUNCATED AT 250 WORDS)
Zhonghua Nei Ke Za Zhi 1995 Apr
PMID:[Dynamic observation of alpha-granule membrane protein 140 during the treatment of thrombolytic and anticoagulant therapy in patients with acute myocardial infarction]. 758 6

Renal vein thrombosis (RVT) was diagnosed in 12 of 60 patients with nephrotic syndrome with CT scan and confirmed by selective renal angiography. Of the 60 patients, 50 had primary glomerulonephritis with various pathological findings and 10 lupus nephritis. CT is valuable in screening renal vein thrombosis. Renal vein and cubital vein blood in the 12 patients were drawn for assay of FDP, AT III, VIIIR: AG, fibrinogen; the results indicated the presence of a state of hypercoagulation. Of these, 7 were given 200,000 units of urokinase (UK) in divided doses into renal vein within one hour and 5,200,000 units UK into renal artery in the same way. Patients also received 2.5mg/d warfarin and 75mg/d persantine. Except for the 3 with focal sclerosis, patients received 40mg/d prednisone. After 1 month CT and blood fibrinogen, FDP, AT III, VIIIR: AG studies were repeated. RVT in patients with intraarterial UK had complete dissolution of their thrombi. Complete dissolution occurred in 2 of the 7 receiving UK by renal vein and there was partial dissolution in the other 5. It seems that intraarterial injection yielded better results. Hypercoagulation state was alleviated in all patients with UK therapy.
Zhonghua Nei Ke Za Zhi 1995 Mar
PMID:[CT examination for renal vein thrombosis in nephrotic syndrome and the effect of thrombolytic therapy]. 764 33

Thrombolytic therapy with intravenous domestic urokinase was carried out within 6 hours after onset in 40 cases of acute myocardial infarction from Feb. 1991 to Dec. 1992, the age of patients being 52.5 +/- 8.4 (37-74) years. The overall reperfusion rate was 65.0%; the reperfusion rate within 3 hours was 78.3% (18/23) and from 3 to 6 hours 47.1% (8/17) (P < 0.05). The incidence of reperfusion arrhythmia was 73.1%. Reinfarction occurred in 3 and acute allergy in 2 cases. 3 other cases developed ventricular fibrillation within 2 hours after onset. After prompt successful defibrillation, thrombolytic therapy was instituted and 2 cases had reperfusion. No marked bleeding and mortality were observed in all of our cases.
Zhonghua Nei Ke Za Zhi 1993 Oct
PMID:[Intravenous thrombolysis with domestic urokinase in 40 cases of acute myocardial infarction]. 815 39

In order to investigate the influences of taurine on thrombolysis serum endothelin (ET) concentration was determined in patients with acute myocardial infarcation (AMI) without urokinase (UK) treatment (group 1) and after treatment with UK (group 2) or UK combined with taurine (group 3). In a rat model with abdominal aorta thrombosed by FeCl3, the changes of serum ET, malodialdehyde (MDA) and intravascular thrombosis were observed in three groups same as in patients. The results were as follows: (1) Serum ET levels of group 1 patients at early phase of onset (6 hours) were significantly higher than those of the controls (47.3 +/- 6.3 ng/L vs 20.4 +/- 9.7 ng/L, P < 0.001). After two days serum ET decreased to normal level. Serum ET levels were significantly higher from 6 to 10 hours after the onset of AMI in group 2 than in group 1 (70.8 +/- 6.6 ng/L vs 56.9 +/- 8.6 ng/L, P < 0.01, at 8 hours). Serum ET levels were significantly lower from 8 hours to a week after onset of AMI in group 3 than in group 2 (33.3 +/- 8.2 ng/L vs 70.8 +/- 6.6 ng/L, P < 0.01, at 8 hours). (2) In the rat model with thrombosis of abdominal aorta, the changes of serum ET were similar to those of AMI patients. In addition serum MDA levels were significantly decreased (20.85 +/- 3.05 mumol/L vs 25.18 +/- 3.53 mumol/L after combined treatment with UK and taurine, P < 0.05). The ratio of cross area of vascular lumen and thrombus was lower after treatment with combination of UK and taurine than treatment with UK alone (0.4650 +/- 0.0928 vs 0.6176 +/- 0.1179, P < 0.05), the results suggested that taurine can decrease significantly serum ET levels, potentiate UK-induced vascular recanlization and reduce ischemia reperfusion injury. Taurine might be useful clinically as an adjunct of thrombolytic therapy.
Zhonghua Nei Ke Za Zhi 1996 Jun
PMID:[Influences of taurine on thrombolysis]. 938 24