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

Fibrin polymers formed from fibrinogen with thrombin in the presence of EDTA were suspended in a medium containing glucose, arabic gum and imidazole-HCl buffer and were sonicated at 20 kHz for 20 min to make a suspension containing fibrin particles of small size. The fibrin suspension was used as a substrate of plasmin for determining the enzymic activity of plasmin and plasminogen activated with urokinase. The kinetic study on the reaction of the fibrin particles with plasmin in the presence and the absence of fibrinogen revealed that Km value of fibrin for plasmin is 4.2 x 10(-7) M and the Ki value of fibrinogen is 1.2 x 10(-5) M.
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PMID:Fibrin suspension as a substrate fop plasmin: determination and kinetics. 16 68

Continuous loss of bile in rats with a bile reservoir applied to the common bile duct caused an increase in specific activity of malic dehydrogenase, lactic dehydrogenase, glutamic dehydrogenase, glucose-6-phosphoric dehydrogenase, alkaline and acid phosphatase, urokinase and histidinase in the liver homogenates by the 7th day; the specific activity decreased by the 10th day. Disruption of innervation of the liver caused a sharp decrease of the ATP content and the abovementioned specifc activity in this organ. In continuous loss of bile there were revealed oscillations in the activity of the above-mentioned enzymes and sorbitol dehydrogenase in bile from the 1st to the 10th day of the experiment. Marked changes in the oscillations in the dysinnervated liver were in favour of the fact that those oscillations coursed under the control of the nervous system.
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PMID:[Enzyme activity of the bile and liver after disruption of its innervation and bile loss]. 18 5

The defibrinating agent ancrod has had limited clinical trial, but appears to give no advantages over heparin. Intravenous infusion of dextran, a glucose polymer, has been shown to have an antithrombotic effect in many experimental models of thrombosis. However, the evidence that dextran is a clinically valuable antithrombotic drug is conflicting. A number of controlled randomized studies have shown that dextran can prevent postoperative venous thromboembolism when a large volume of dextran 40 or 70 was infused rapidly during and after surgery. However, blood volume expansion during dextran treatment prohibits its use in patients with reduced cardiac reserve, and infrequent though sometimes severe, allergic reactions have been reported. Evidence that dextran is of value for the treatment of venous or arterial thromboembolism comes from uncontrolled studies and is not convincing. Many compounds have been shown to inhibit platelet function in vitro but only five of these drugs have been extensively evaluated as prophylactic or therapeutic antithrombotic agents in man. These are aspirin, sulphinpyrazone, dipyridamole, hydroxychloroquine and clofibrate. They have been evaluated mainly in patients with cerebral vascular disorders, coronary artery disease, peripheral artery ischaemia, venous thromboembolism, prosthetic heart valves, and in patients with arteriovenous shunts. The evaluation of the clinical effect of the platelet function suppressing drugs is in its early stages, but they appear to differ from each other in the spectrum of their clinical effectiveness, and they may be more effective in arterial than in venous thromboembolic disorders. Their role in the management of cerebral vascular disease and coronary artery disease is still uncertain, and should be clarified by the results of a number of multi-centre, prospective, randomized studies which are currently in progress. Three types of thrombolytic drugs have been evaluated clinically; the plasminogen activators streptokinase and urokinase, proteolytic enzymes such as plasmin, and agents which increase the level of endogenous plasminogen activator (e.g. anabolic steroids). Of these, the plasminogen activators now have a definite place in clinical practice. The plasminogen activators accelerate the lysis of recent venous thrombi and pulmonary emboli, and of arterial thrombi or emboli. Thrombolytic therapy with these agents should be considered particularly in patients with recent major pulmonary embolism, as lysis of recent emboli is rapid and substantial. It should also be considered in patients with recent extensive venous thrombosis, because total lysis of venous thrombi has been reported to result in long-term preservation of valve function, and is likely to prevent postphlebitic syndrome, though this has not been proven. However, plasminogen activator therapy carries a higher risk of bleeding than heparin treatment...
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PMID:Antithrombotic drugs: part II. 78 6

In the United States, approximately one million patients each year develop a pleural effusion. Pleural effusions have classically been divided into transudative and exudative pleural effusions. A transudative pleural effusion occurs when the systemic factors influencing pleural fluid formation and reabsorption are altered so that pleural fluid accumulates; an exudative pleural effusion occurs when the local factors influencing pleural fluid formation and reabsorption are altered, allowing accumulation of pleural fluid. The leading causes of transudative pleural effusions are left ventricular failure and cirrhosis with ascites. The leading causes of exudative pleural effusions are pneumonia, malignancy, and pulmonary embolization. Transudative pleural effusions can be differentiated from exudative pleural effusions by measurement of the pleural fluid protein and lactic dehydrogenase (LDH) levels. The ratio of the pleural fluid protein to the serum protein is less than 0.5, the ratio of the pleural fluid LDH to the serum LDH is less than 0.6, and the absolute value of the pleural fluid LDH level is less than two thirds of the upper normal limit for serum with transudative pleural effusions while at least one of these criteria is not met with exudative effusions. Most patients who have a pleural effusion with congestive heart failure have left ventricular failure. It is believed that the transudation of the pulmonary interstitial fluid across the visceral pleura overwhelms the capacity of the lymphatics to remove the fluid. Most patients with cirrhosis who have a pleural effusion also have ascites. It is also believed that the pleural effusions form when fluid moves directly from the peritoneal cavity into the pleural cavity through pores in the diaphragm. Approximately 40% of patients with pneumonia will have a pleural effusion. If these patients have a significant amount of pleural fluid, a diagnostic thoracentesis should be performed. Chest tubes should be inserted if the pleural fluid is gross pus, if the Gram stain of the pleural fluid is positive, if the pleural fluid glucose level is below 40 mg/dl, or if the pleural fluid pH level is less than 7.00. If drainage with the chest tubes is unsatisfactory, either streptokinase or urokinase should be injected intrapleurally. If drainage is still unsatisfactory, a decortication should be considered. The three leading malignancies that have an associated pleural effusion are breast carcinoma, lung carcinoma, lymphomas and leukemias. The diagnosis of pleural malignancy is made most commonly with pleural fluid cytology; in recent years immunohistochemical tests have proved invaluable in differentiating benign from malignant pleural effusions.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Pleural diseases. 157 32

The stabilities of urokinase (UK) in aqueous solution were investigated at pH 5.0-8.0 in the presence (1.0-3.0 x 10(-3) M) and absence of sodium bisulfite (SBS) both under scattered light (1000 lux) and in the dark using the fluorogenic substrate method. Increasing concentrations of SBS tended to increase the inactivation of UK. In the presence of SBS, with the increase in the pH value, UK gained in stability in the pH range of 5.0-8.0. The stability of UK in the presence of SBS in the dark was larger than that under scattered light, especially at pH 5.0. Therefore, it was suggested that the difference in the residual activities of UK between under light and in the dark was due to free radicals formed during the autooxidation of bisulfite under scattered light. UK was stabilized by glucose in the presence of SBS both under scattered light and in the dark. One reason for this phenomenon was postulated to be the formation of inactive bisulfite-glucose addition compound. The degradation products of UK during storage in a solution containing SBS were investigated by sodium dodecyl sulfate (SDS)-polyacrylamide gel electrophoresis. UK was revealed to be split into M.W. 36000 form and M.W. 20000 form by SBS.
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PMID:Stability of urokinase in solutions containing sodium bisulfite. 220 81

A method of assay for glycated fibrinogen (C-Fbg) in plasma has been developed. This method is based on the measurement of 1-deoxy-1-morpholino-D-fructose (DMF) in the fibrinogen (Fbg) solution separated from plasma and redissolved. Twenty five NIH units of thrombin was added to 600 microliters of plasma. After incubation, the fibrin clot was separated and washed. The fibrin clot was redissolved with Owren's veronal buffer contained urokinase. After incubation, DMF was measured using a Fructosamine Kit. G-Fbg measured by this method correlated significantly with the amount of furosine that was a specific product by hydrolysis of glycated lysine residue. In this method, the CV for intraday assay ranged from 2.0 to 3.6% and that for interday assay was 3.9%. The average of G-Fbg values in 78 diabetic patients (23.8 +/- 10.7 mumol DMF/g Fbg) was significantly higher than in 26 normal subjects (9.2 +/- 3.8 mumol DMF/g Fbg). The G-Fbg value correlated with blood glucose at the same time or one day earlier than 1-2 weeks or 1 month earlier. These results suggest that assay of G-Fbg by this method may be useful in monitoring short-term control of blood glucose in diabetic patients.
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PMID:[Assay of glycated fibrinogen in plasma as an indicator of blood glucose control]. 234 67

The rate of glucose-stimulated insulin release was found to be increased but that of proinsulin conversion decreased in islets removed from diazoxide-treated rats. This coincided with an elevated islet proinsulin/insulin ratio. The defect in proinsulin conversion was not corrected by preincubating the islets, at high glucose concentration, in the presence of either urokinase or rat serum. Likewise, the administration of kallikrein inhibitor in vivo did not affect the rate of proinsulin conversion as measured in vitro. Since these results fail to document a role for exocytosis-coupled endocytotic uptake of circulating factors in the efficiency of proinsulin conversion, it is speculated that the slackening of the latter process in islets removed from diazoxide-treated rats could be somehow linked to sustained inhibition of insulin release.
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PMID:Diazoxide-induced long-term hyperglycemia. II. Slackening of proinsulin conversion. 266 20

A study on the significance of the measurement of fibrinopeptide A (FPA) and fibrinopeptide B beta 15-42 (FPB beta) in urine and plasma before and after urokinase (UK) administration in patients with chronic glomerulonephritis is described. FPA and FPB beta in urine and plasma were measured by radioimmunoassay. The levels of fibrinogen degradation product (FDP) in urine and sera were also determined before and after the UK administration. UK was administered at a dose of 48,000 IU/20 ml in saline intravenously, followed by an intravenous infusion of 250 ml of 5% glucose for one hour. It was demonstrated that the levels of FPB beta in urine and plasma showed a significant increase after UK administration in patients with chronic glomerulonephritis. However, there was no significant difference in the levels of FDP in urine and sera before and after UK administration. It was concluded that the measurement of FPB beta in urine and plasma may be useful for evaluating the efficacy of UK therapy in patients with chronic glomerulonephritis.
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PMID:Levels of fibrinopeptide A (FPA) and fibrinopeptide B beta 15-42 (FPB beta) in urine and plasma after urokinase administration in patients with chronic glomerulonephritis. 361 11

MCI-2016 showed little influence on coagulation (APTT) and fibrinolysis (plasma clot lysis activated by urokinase) at doses (concentrations) as high as 300 mg/kg, p.o. or 8.6 X 10(-4) M. Hemolytic action of MCI-2016 was only observed at the concentrations above 2 mM. The drug also showed no influence on blood glucose level (30-300 mg/kg, p.o.). Effects of MCI-2016 on hemorheological properties were studied either in vitro or ex vivo. Above the doses (concentrations) of 100 mg/kg, p.o. and 10 microM, MCI-2016 suppressed the mechanical hemolysis and accelerated the membrane filtration rate. These effects of MCI-2016 were superior to those of cinepazide, Ca-hopantenate, meclofenoxate and pentoxyfylline. MCI-2016 also inhibited platelet aggregation induced by collagen with the IC 50 of 35 to 60 microM (rabbit and human platelets). Secondary aggregations of ADP and epinephrine were also inhibited by MCI-2016. As for reference drugs, bencyclane showed inhibitory patterns similar to MCI-2016. Other drugs examined exhibited little effect. In summary, it may be suggested that MCI-2016 exhibits beneficial influences in the clinical fields of cerebrovascular diseases.
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PMID:[Effects of 4-(o-benzylphenoxy)-N-methylbutylamine hydrochloride (MCI-2016, bifemelane hydrochloride) on coagulation, fibrinolysis, hemolysis, hemorheological properties and platelet aggregation]. 369 29


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