Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.68 (tissue plasminogen activator)
 11,311 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Endothelial release of tissue plasminogen activator (t-PA) may initiate fibrinolysis. Fibrinolysis and coagulation were investigated in 12 patients undergoing elective coronary artery bypass surgery. Cardiopulmonary bypass (CPB) was 108 +/- 7 min (mean +/- SEM), the time of cold, crystalloid, retrograde cardioplegia 53 +/- 5 min. Arterial and coronary sinus blood were sampled concomitantly before cardioplegia and after release of the aortic cross-clamp, for measurement of t-PA antigen (Ag) and activity, plasminogen activator inhibitor (PAI-1) Ag and activity, t-PA/PAI-1 complex, single chain urokinase (sc-uPA) and urokinase (uPA) plasminogen activators, the fibrin split product D-dimer, thrombin-antithrombin complex (TAT), and the prothrombin split product F 1 + 2. Cardiopulmonary bypass significantly increased t-PA Ag and activity, t-PA/PAI complex, D-dimer, TAT, and F 1 + 2, and decreased PAI-1 Ag and activity in arterial blood; uPA and sc-uPA were unchanged. The tissue plasminogen activator antigen was higher in coronary sinus than arterial blood after 1 (39 +/- 5 vs 24 +/- 4 ng/ml, P < 0.003), 4 (P < 0.003), and 10 min (P < 0.004) reperfusion. Tissue plasminogen activator activity and t-PA/PAI complex increased, PAI-1 activity decreased, while all other parameters were unchanged across the coronary circulation. In conclusion, CPB induces fibrinolysis and coagulation. Cold cardioplegia induces t-PA release in the coronary circulation, denoting a postischemic antithrombotic function of the coronary endothelium. Tissue plasminogen activator may be used to evaluate endothelial stimulation or injury induced by CPB, or by different regimens of myocardial protection.
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PMID:Fibrinolysis during cardiac surgery. Release of tissue plasminogen activator in arterial and coronary sinus blood. 808 78

To explore the role of transforming growth factor-beta (TGF beta) isoforms and other growth-related genes during prostate morphogenesis in the mouse, we examined mRNA levels in fetal day 17 urogenital sinus, mesenchyme (UGM), and epithelium (UGE) as well as in the ventral, dorsal, and anterior lobes of the adult prostate. In addition, we used antiserum specific for extracellular TGF beta 1 in immunohistochemical studies to localize accumulation of the TGF beta 1 isozyme in the above tissues as well as those derived from fetal day 19 and neonatal mouse prostate. Differential patterns of expression in fetal and adult tissues were seen. TGF beta 1, -beta 2, and -beta 3 expression was substantially elevated in UGM compared to that in UGE, yet only TGF beta 1, not TGF beta 2 or TGF beta 3, mRNA levels were sustained in adult prostate tissues. High levels of accumulation of TGF beta 1 were demonstrated by immunohistochemistry in the mesenchymal compartment compared to those in the epithelial compartment throughout development. Interestingly, the highest levels of TGF beta 1 appeared in areas of active epithelial duct formation and delineated the mesenchymal architectural changes necessary for ductal network formation. Additional studies revealed that levels of mRNAs for other genes involved in tissue remodeling and growth were also elevated in UGM compared to those in UGE. Tissue plasminogen activator, urokinase plasminogen activator, androgen receptor, and c-myc mRNA levels were also elevated in UGM compared to UGE. Interestingly, whereas tissue plasminogen activator mRNA levels, like those of TGF beta 2 and -beta 3, were barely detectable in adult prostatic tissues, mRNA levels for urokinase plasminogen activator, androgen receptor, and c-myc were readily detected and expressed in a lobe-specific fashion. Overall, these data indicate that expression of TGF beta 1 isoforms and other growth-related genes is associated with mesenchymal cells in areas of active morphogenesis during prostate development and provide objective molecular and cellular information regarding mediators of mesenchymal-epithelial interactions in prostate.
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PMID:Mesenchymal-epithelial interactions and transforming growth factor-beta expression during mouse prostate morphogenesis. 811 40

The aim of this study was the evaluation of the in vitro production of prostacyclin, and of tissue plasminogen activator (tPA) and its inhibitor, PAI-1, by human endothelial cells cultured in the presence of polyethylene terephthalate (PET). After a 48 h contact between the cells and the polymer, the concentration of 6-keto-PGF1 alpha, a stable metabolite of prostacyclin, tPA, and PAI-1, was assayed on the supernatants. Contact of the endothelial cells with PET produced a highly significant reduction of 6-keto-PGF1 alpha with respect to control cultures. Tissue plasminogen activator concentration in the supernatants of the cultures in contact with the material was similar to that observed in the controls, while PAI-1 production was significantly reduced. It can be concluded that the contact between endothelial cells and PET determines a reduction in the platelet aggregability and an increase of the fibrinolytic activity due to a decrease in PAI-1, while tPA concentration remains unchanged.
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PMID:Production of prostacyclin and fibrinolysis modulators by endothelial cells cultured in the presence of polyethylene terephthalate. 812 14

We studied extrinsic and intrinsic fibrinolysis in 20 patients with cirrhosis (nine mild/moderate, group 1; 11 severe, group 2) and 19 normal controls to define the role of intrinsic (contact factor medaited) fibrinolysis in cirrhosis. Global plasma fibrinolytic activity (fibrin plate lysis) was similar in all groups. Dextran sulphate activated contact factor mediated fibrinolysis was decreased in group 2 (median 95.2%) compared with group 1 (121.0%) and controls (131.7%). Tissue plasminogen activator antigen (t-PA Ag) levels were increased in group 2 (28.2 ng/ml) compared both with group 1 (8.5 ng/ml) and controls (5.9 ng/ml). Plasma t-PA activity was raised in group 2 (5.50 IU/ml) and group 1 (5.25 IU/ml) versus controls (0.82 IU/ml). Plasminogen activator inhibitor-1 (PAI-1 Ag) levels were raised in group 2 (28.0 IU/ml) versus controls (8.5 IU/ml) but PAI activity was similar in all groups. Factor XII activity was decreased in group 2 (48.76 u/dl), but not group 1, versus controls (89.1 u/dl). Prekallikrein activity was decreased both in group 2 (27.27 u/dl) and group 1 (33.01 u/dl) versus controls (108.59 u/dl) and was lower in group 2 than group 1. C1-esterase inhibitor chromogenic activity was decreased in group 1 (102.30 u/dl) and group 2 (58.76 u/dl) versus controls (116.24 u/dl). The normal global fibrinolytic activity despite increased t-PA activity may be due to a concomitant increase in PAI. The decreased intrinsic fibrinolysis in severe cirrhosis, unaccompanied by a rise in C1-esterase inhibitor, may be explained by the decreased factor XII and prekallikrein activity. These changes are probably due to reduced liver cell mass.
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PMID:Decreased contact factor mediated fibrinolysis in cirrhosis. 813 76

Haemorrhagic diathesis is a serious complication of uraemia. Desmopressin is known to shorten prolonged bleeding time in uraemia but mechanism of the haemostatic action of this drug remains still unknown. The aim of the work was to study the effect of desmopressin on some haemostatic parameters in relation to plasma and platelet serotonin. Desmopressin was administered i.v. to 33 haemodialysed patients (age range 27-66 years) in a dose of 0.4 microgram/kg b.w., 90 minutes after desmopressin infusion bleeding time became significantly shorter (p < 0.001) and correlated with the shortening of the euglobulin clot lysis time (r = -0.43, p < 0.05). Tissue plasminogen activator activity increased (p < 0.01) and its inhibitor (PAI) activity decreased (p < 0.001) after desmopressin infusion. A correlation between the fall in platelet serotonin content and changes in tissue plasminogen activator and PAI activities was found (r = 0.55, p < 0.01 respectively). A rise in plasma serotonin concentration was observed. In vitro desmopressin inhibited 14C serotonin uptake in a dose-dependent manner. After 2 hours of platelet incubation with desmopressin in a concentration of 4 ng/ml 16% of 14C serotonin was released. A possibility of serotoninergic mechanism in the haemostatic action of desmopressin is suggested.
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PMID:[Possible role of serotonin in hemostatic the mechanism of action of desmopressin (DDAVP) in patients with uremia]. 824 43

Stroke outcome is measured by survival and disability. Since more patients are surviving stroke, researchers are pursuing ways to reduce the severity of neurological deficits. Anticoagulant treatment with heparin prevents, rather than treats, thrombotic or embolic occlusions; therefore, the search for safer thrombolytic preparations continues. Tissue plasminogen activator is currently under investigation as an effective, safe treatment for acute stroke patients. However, the administration of tPA carriers a risk of hemorrhage. Although this article discussed tPA administered with an arteriogram based protocol, tPA investigation occurs using other protocols. Once acute stroke patients receive tPA, then measures to prevent complications and manage the stroke symptoms determine the risks and benefits patients receive. Nursing management of these patients can contribute to these benefits.
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PMID:tPA in acute stroke--risk or reprieve? 834 Jun 40

Fibrinolytic activity and tissue plasminogen activator (t-PA) level were measured in 33 healthy individuals prior to and after fibrinolytic system stimulation (i.e. a ten-minute venous stasis). Fibrinolytic activity was measured with the aid of euglobin lysis time, and lysis test on the fibrin plates (in own modification). Tissue plasminogen activator concentration was assayed spectrophotometrically with the COA-SET t-PA (Kabi Vitrum). No fibrinolytic activity of plasma specimens taken before the venous stasis was noted during fibrin lysis plate test whereas it was seen in 13 subjects after the venous stasis. Fibrinolytic activity of the plasma euglobins, measured as a surface on fibrin plates, increased significantly after the venous stasis in both sexes (by 35.5 mm2 on the average, i.e. by 51%). It was more marked in men than in women both prior to and after venous stasis (by 10.9% and 19.0%, respectively). A time of plasma euglobin lysis was shorter after venous stasis (by 110 minutes, on the average). There was no significant difference between the sexes. Tissue plasminogen activator concentration increased by 5.8 times (from 1.7 IU/ml to 9.9 IU/ml) after the stasis. Correlation between t-PA concentrations and fibrinolytic activity, measured on the fibrin plates, was highly positive. No such a correlation existed between t-PA concentrations and the time of euglobin lysis. The obtained results indicate variety of assessments of fibrinolytic system activity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Fibrinolytic activity and tissue plasminogen activator level in healthy individuals prior to and after a ten-minute venous stasis]. 836 5

This study explored the relationship between clotting activation and tissue plasminogen activator and its inhibitor in cirrhotic patients with different degrees of liver failure. Sixty-seven patients (40 men, 27 women; age = 31-77 yr) with cirrhosis diagnosed by liver biopsy were divided into three subgroups (A, B and C) on the basis of Child-Pugh classification. Tissue plasminogen activator antigen and activity, plasminogen activator inhibitor antigen and activity, fibrin/fibrinogen degradation products, and D-dimer were measured in each patient. Forty-two patients with normal levels of fibrin/fibrinogen degradation products and D-dimer showed significant progressive decreases of plasminogen activator inhibitor antigen levels (p < 0.01) and activity (p < 0.0001) from class A to class C. This decrease was significantly related to prothrombin time (p < 0.003). Tissue plasminogen activator values were not different in the three Child classes. Twenty-five patients (7 class B and 18 class C) with high circulating values of fibrin/fibrinogen degradation products and D-dimer had higher values of tissue plasminogen activator antigen (20.0 +/- 10.1 ng/ml vs. 5.9 +/- 3.0 ng/ml; p < 0.0001) and activity (6.9 +/- 2.2 U/ml vs. 2.1 +/- 1.3 U/ml; p < 0.0001) and lower values of plasminogen activator inhibitor antigen (6.9 +/- 4.1 ng/ml vs. 14.8 +/- 5.6 ng/ml; p < 0.0001) and activity (4.1 +/- 2.8 U/ml vs. 9.8 +/- 3.7 U/ml; p < 0.0001) than did patients with normal values of fibrin/fibrinogen degradation products and D-dimer.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperfibrinolysis resulting from clotting activation in patients with different degrees of cirrhosis. The CALC Group. Coagulation Abnormalities in Liver Cirrhosis. 842 44

Fluctuations in tissue plasminogen activator (t-PA) activity, t-PA antigen, and plasminogen activator inhibitor-I (PAI-1) antigen levels were evaluated in blood samples obtained from 84 patients with initial uneventful acute myocardial infarction (AMI) and 35 patients with reinfarction and fatal infarction (patients with bad prognoses). Patients with initial AMI had significantly higher levels of t-PA activity than those of 14 patients with angina pectoris. Tissue plasminogen activator activity peaked between day 7 and 19 after the initial attack of AMI. Plasminogen activator inhibitor-I antigen level decreased significantly between day 2 and 19, then returned to the baseline levels of patients with angina pectoris nearly 4 weeks later. The t-PA activity levels of patients with reinfarction were significantly lower than those in patients without events between day 0 and 3 and between day 7 and 19. The percentage stenosis in the coronary arteries measured by coronary angiography was negatively correlated with t-PA activity. This information may help in selecting aggressive treatments such as thrombolysis by recombinant t-PA and predicting the prognosis for patients with AMI.
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PMID:Evaluation of tissue plasminogen activator and plasminogen activator inhibitor-I levels in acute myocardial infarction. 864 3

Tissue plasminogen activator activity in the developing cerebellum, as quantified by zymography of cerebellar homogenates from embryonic day (E) 17 to adult mice, shows a peak of activity at postnatal day (P) 7, followed by a steady 75% decrease into adulthood. Northern blot analysis reveals a similar pattern for tissue plasminogen activator mRNA levels, which are low at E17 but increase dramatically, reaching their highest levels of specific mRNA/micrograms RNA in P1-P7 mice and declining about threefold in the adult mouse. In situ hybridization of whole mouse brain sections with a tissue plasminogen activator antisense cRNA probe shows pronounce reactivity in the cerebellum. Although some binding is associated with the cerebellar meninges, the external granule layer is devoid of tissue plasminogen activator mRNA at all ages. However, highly labeled elongated cells, which also bind antibody to neuronal nuclear antigen and are adjacent to Bergmann glial fibers (i.e., migrating granule neurons), are readily visible throughout the molecular and Purkinje layers at P7 and P14. In the adult mouse cerebellum, tissue plasminogen activator mRNA labeling is restricted to cells in the Purkinje/internal granule layers. Thus, tissue plasminogen activator gene expression is induced as granule neurons leave the external granule layer and begin their inward migration.
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PMID:Tissue plasminogen activator mRNA expression in granule neurons coincides with their migration in the developing cerebellum. 880 Dec 57


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