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

341 patients with acute myocardial infarction have been treated in intensive or coronary care units. They were randomised into two groups, 172 receiving urokinase and 169 receiving a glucose infusion. Thereafter they were anticoagulated first with heparin and then for a year with oral anticoagulants. Despite a significantly faster regression of electrocardiographic alterations in the urokinase group there was no difference in mortality during the 1-year follow-up (29 deaths in the urokinase and 24 in the control group) and no difference in cardiac functional class between both groups.
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PMID:Controlled trial of urokinase in myocardial infarction. A European Collaborative Study. 5 1

20 patients (6 females, 14 males) aged between 47 and and 75 years (mean: 62.6 yrs.) with acute myocardial infarction (onset of symptoms within 6 hours) were treated intravenously with either 200,000 U urokinase (UK) and 4.5 million U pro-urokinase (pro-UK) within 60 min (group I, N = 10), or 2.5 million U UK within 5 min (group II, N = 10). Blood samples for haemostatic and fibrinolytic function tests were taken prior to and repeatedly during the 24 hours following treatment. Peak fibrinolytic activity measured by fibrin plates was equivalent in both regimens. Average decreases, with lowest levels within 60 to 120 min following thrombolytic therapy, were observed of 27% and 70% for plasminogen, of 71% and 91% for alpha-2-antiplasmin, and of 20% and 74% for fibrinogen in group I and II, respectively. The reptilase time reached maximum values of 1.5- and 4.5-fold within 60 to 180 min. Peak levels of D-dimers and thrombin-antithrombin III complexes in group II were 2.6 and 3.2 times those of group I. After 24 hours, in contrast to group I, all these parameters still remained significantly different from pretreatment values in group II. These data indicate that, contrary to high-dose UK, pro-UK in combination with low-dose UK causes minor systemic fibrinolytic effects and is, therefore, assumed to be largely clot-specific, although the fibrinolytic potential is equivalent for both regimens.
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PMID:Fibrinolytic effects of pro-urokinase combined with low-dose urokinase compared to high-dose urokinase in patients with acute myocardial infarction. 127 35

Thrombolysis has been reported to restore coronary blood flow in patients with acute myocardial infarction (AMI). However, the relationship between fibrinolytic treatment and evidence of myocardial reperfusion has not been adequately assessed. Accordingly, we measured great cardiac vein blood flow (GCVF:thermodilution) in 12 patients (Group 1) presenting with AMI (chest pain < 4 hours and ST elevation in the anterior leads) before and following i.v. urokinase (UK:2 million U/90 min). Ten patients receiving conventional treatment served as controls (Group 2). UK induced a significant increase of GCVF (from 101 +/- 24 to 164 +/- 42 ml/min, p < 0.001). Maximal increase occurred after 50 +/- 54 min from drug infusion. Conversely, changes in GCVF were not significant in Group 2 (from 103 +/- 35 to 106 +/- 31 ml/min, NS). Following 24 hours changes in GCVF were still consistent only in Group 1 patients. Individual analysis during 24 hours showed marked fluctuations of GCVF peak values in Group 1 patients (62 +/- 43%), but not in Group 2 (29 +/- 21%). Thus, UK induces a marked increase of GCVF in most patients with anterior AMI; such increase suggests that reperfusion occurs early (i.e. within 1 hour) from UK administration. Fluctuations of GCVF during monitoring are magnified by thrombolysis, suggesting intermittent coronary reocclusion in the early hours of AMI.
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PMID:[Regional coronary blood flow in patients with acute myocardial infarct treated by systemic fibrinolysis]. 129 51

Acute myocardial infarction (AMI) is one of the most intractable diseases and is increasing rapidly in Japan and China. Two hospitals in Japan and China, the Critical Care Center of Kurume University Hospital and the Chinese Beijing 309 Hospital in China (abbreviated to Beijing 309 Hospital) were compared. The incidence, mortality and treatment of AMI were investigated in both hospitals from 1989 to 1991. The incidence of AMI for all patients admitted during the three years was 5% in Kurume University Hospital and 4.7% in Beijing 309 Hospital, which are similar rates. The average age of the patients in Beijing 309 Hospital was younger (58 +/- 13) than in Kurume University Hospital (64 +/- 11). The mortality rate in Kurume University Hospital was slightly lower than the rate in Beijing 309 Hospital (8.1% vs 8.9%). Thrombolytic therapy was actively performed in both hospitals. In Kurume University Hospital, urokinase (UK: 71.4%) or recombinant tissue plasminogen activator (rt-PA: 28.6%) was administered by intravenous (85.7%) and intracoronary percutaneous transluminal coronary recanalization (PTCR: 14.3%) injection. In Beijing 309 Hospital, UK (32.7%) or snake poison enzyme (SPE: 62.3%) was administered by intravenous (85.8%) or intra-aortic (14.2%) injection. Rt-PA was only used in Japan and SPE was only used in China, but both had very strong fibrinolytic effects and resulted in high success rates of coronary reperfusion. The incidence of direct coronary intervention with percutaneous transluminal coronary angioplasty (PTCA) and intra-aortic balloon pumping (IABP) for cardiogenic shock was much higher at Kurume University Hospital than at Beijing 309 Hospital.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Comparison of incidence, mortality and treatment of acute myocardial infarction in hospitals in Japan and China. 130 10

Creatine kinase(CK), aspartate aminotransferase (AST), alpha-hydroxybutyrate dehydrogenase (HBDH), lactate dehydrogenase (LD) and LD isoenzymes, CK-MB isoenzymes and CK-MM isoforms were measured in 17 acute myocardial infarction (AMI) patients treated with thrombolysis resulting in reperfusion and 2 not resulting in reperfusion as well as 71 treated conventionally to assess reperfusion. The results showed that the peak of the ratio of MM3 to MM1 was attained significantly earlier in patients with reperfusion than in those conventionally treated and those without reperfusion, and this ratio is considered to be a good indicator to assess reperfusion. The results were similar to those of previous reports. The peak in all the 17 patients with confirmed reperfusion was attained within 9 hours after onset of AMI, while only 9 of the 73 patients in the group without reperfusion had their peaks within 9 hours. The diagnostic efficiency was 94%. The authors suggested a new indicator for assess reperfusion. An increase of CK-MM3 over 10% from the first to the second hour after treatment with urokinase was found in 15 of the 17 urokinase-treated patients with reperfusion. The diagnostic efficiency was also 94%. We consider that it is an indicator as good as the peak of ratio of MM3/MM1. Furthermore, with this indicator, it is possible to assess reperfusion in two hours after treatment with urokinase.
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PMID:[Determination of serum creatinine kinase MM isoforms in assessing reperfusion after acute myocardial infarction]. 131 15

In the past 10 years, thrombolytics have become standard therapy for acute myocardial infarction. Although the ability of streptokinase to lyse clot was first recognised in the 1930s, thrombolytic therapy was not used to treat acute myocardial infarction until the early 1980s, when the importance of thrombosis in the pathogenesis of acute infarction was fully recognised. In addition to streptokinase and urokinase, recombinant human tissue plasminogen activator (tPA) and anistreplase were developed and widely used in the 1980s. Saruplase (prourokinase) and BM-06022 (recombinant plasminogen activator) have also undergone human clinical studies. All of these agents are effective at achieving clot lysis and coronary patency. Large, randomised clinical trials have demonstrated that thrombolytic therapy reduces mortality in patients with ST elevation treated within the first 6 to 12 hours of acute infarction, with an approximately 0.5% risk of intracranial haemorrhage. Recent data have more clearly identified which patients benefit from thrombolytic therapy. Efforts have been made to improve the speed of reperfusion, decrease reocclusion, simplify administration and reduce adverse effects. The characteristics of fibrin specificity and more rapid clot lysis with tissue plasminogen activator have not yet been translated into overall clinical benefit compared with the less expensive streptokinase. The lack of close association of improved early patency and improved global left ventricular function with improved survival challenges the very paradigm which led to the use of thrombolytic therapy for acute myocardial infarction. The need for development of additional methods for evaluation of new thrombolytic agents is evident.
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PMID:Thrombolytic therapy for acute myocardial infarction. A review . 138 31

Coronary thrombolysis reduces morbidity and mortality in patients with acute myocardial infarction, however, the exact effects of thrombolytic agents on the status of intrinsic hemostases are not fully understood. In the present study, we examined serial changes in plasma thrombin and protein C activities of 6 patients with acute myocardial infarction treated with urokinase. Fibrinolysis occurred immediately after urokinase injection with an increase in the plasma thrombin-antithrombin III complex, suggesting a subsequent procoagulant state due to thrombin generation. Correspondent increases in plasma protein C activity were observed, however, protein S levels did not change at all. Our findings suggest that urokinase administration for coronary thrombolysis not only causes fibrinolysis, but also induces thrombin activity, which may be antagonized by augmented intrinsic protein C activity.
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PMID:Augmented plasma protein C activity after coronary thrombolysis with urokinase in patients with acute myocardial infarction. 138 46

Four hundred and one patients with acute myocardial infarction of less than 4 h duration were randomized to receive intravenous thrombolytic treatment with either 80 mg of full length unglycosylated single-chain-urokinase plasminogen activator (INN saruplase) or 1.5 million IU of streptokinase delivered over a 60 min period. Angiographic patency rates were higher at 60 min in saruplase treated patients (71.8% vs 48%; P less than 0.001), but did not differ significantly at 90 min (71.2% vs 63.9%; P = 0.15). Fibrinogen levels dropped markedly in both groups, the decrease being delayed and less pronounced with saruplase. Total fibrin and fibrinogen degradation products and D-dimer values rose earlier and to higher peak values in streptokinase treated patients. In both groups marked plasminogen and alpha 2-antiplasmin consumption was observed. Lower fibrinogen levels, and in particular the faster rate of fibrinogen breakdown, were associated with higher patency rates at 90 min (P less than 0.05). Patients with bleeding complications had lower 'lowest points' and a more rapid decrease in fibrinogen (P less than 0.05). These findings were not related to the drug used. Increased heparin levels at 6 to 12 h were correlated to bleeding complications in streptokinase treated patients. It is concluded that the rate of fibrinogen breakdown during and following thrombolytic treatment for acute myocardial infarction is related to early vessel patency and bleeding complications.
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PMID:Rate of fibrinogen breakdown related to coronary patency and bleeding complications in patients with thrombolysis in acute myocardial infarction--results from the PRIMI trial. 139 33

Thrombolytic therapy using recombinant-tissue plasminogen activator, urokinase and streptokinase for acute myocardial infarction was instituted in the coronary care unit of the Prince of Wales Hospital in Hong Kong in 1988. To evaluate its impact on hospital mortality of acute myocardial infarction, the database of 465 patients (mean age 65.2 +/- 12.6 yr) admitted into the coronary care unit in the period between 1985-1990 was collected prospectively and their clinical course reviewed. Three hundred and thirty-five patients were males and 130 were females. Patients in the prethrombolytic era (1985-87) and the thrombolytic era (1988-90) were matched for age, proportion of females and clinical severity. One hundred and two patients (39.5%) received thrombolytic therapy. The overall hospital mortality (18.6%) in the thrombolytic era and that for each sex (18.2% in the males; 19.5% in the females) were significantly lower than those of prethrombolytic era (27.1%, 23.4% and 37.7%, respectively). No death was due to bleeding complication. The benefit of thrombolytic therapies in the Chinese was confirmed. More effort is needed to popularize this concept in the Chinese communities, to shorten the prehospital delay of patients and to extend its utilisation to the elderly patients.
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PMID:The impact of thrombolytic therapy on hospital mortality from acute myocardial infarction in the Chinese in Hong Kong. 145 73

Intracoronary thrombodynamics in acute coronary syndromes was studied with an experimental canine model. An intracoronary thrombus was precipitated at the mock ruptured atheromatous plaque consisting of cholesterol and collagen. In 8 of 10 control models, acute myocardial infarction (AMI) was induced by intracoronary occlusive thrombus 1 h after the start of the experiment. Coronary blood flow decreased continuously (Type A, n = 5) or cyclically (Type B, n = 3) to end in AMI. Effects of pharmacological interventions to prevent AMI were also studied with the model. An intravenous bolus injection of a thromboxane synthetase inhibitor (RS-5186), heparin, a thrombin inhibitor (argatroban), and a thrombolytic agent (urokinase) was performed in 10 models for each drug. The incidence of AMI was significantly decreased to 3 of the 10 models injected with the thromboxane synthetase inhibitor and heparin (p < .05, each drug group vs. control). The preventive effect of argatroban was more potent and AMI occurred in 2 of 10 models (p < 0.01, argatroban vs control).
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PMID:Experimental evaluation of coronary thrombodynamics and effects of pharmacological interventions in acute coronary syndromes. 145 44


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