Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P00750 (PLA)
 16,800 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A newly developed low molecular weight heparin (LU 47311) was given to 6 healthy volunteers (males, mean age: 30.5 years, range: 20-39 years). They obtained a single dose of 40 and 60 anti FXaU per kg body weight, respectively, by subcutaneous administration. The anti FXa elimination half-life was close to 3 hours. The APTT showed slight response following high dose. No significant influence on fibrinolysis as measured by t-PA and PAI assays was noticed. There was no clear evidence of enhancement of platelet function when detected by Born's method and platelet factor 4 and beta-thromboglobulin assays. However, a moderate but significant increase of thromboxane B2 was noticed in the group obtaining an elevated dose of LMW heparin. Serum levels of triglycerides and cholesterol remained unaltered. The aminotransferases, electrolytes, renal function parameters and cell counts of the peripheral blood were not influenced by LMW heparin.
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PMID:Study of a new low molecular weight heparin (LU 47311) administered to healthy volunteers. 248 3

Corneal epithelial cells secrete tissue plasminogen activator (t-PA), urokinase type plasminogen activator (u-PA) and their inhibitor (PAI), whereas these cell types in other tissues are known to secrete only u-PA hitherto. Endothelial cells in the cornea produce mostly u-PA and only small amounts of t-PA and PAI which remain confined in the cellular compartment contrary to the situation in the vascular endothelial cells where they are liberated into the circulation in the order PAI greater than t-PA greater than U-PA. These unique features of activator/inhibitor secretion and production may play an important role in the remodeling of the corneal matrix.
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PMID:Production of proteases type plasminogen activator and their inhibitor in cornea. 249 21

Defibrotide, an antithrombotic drug, was previously shown to activate fibrinolysis. In order to elucidate the relationship between defibrotide treatment and fibrinolysis, ten atherosclerotic patients were given 1200 mg/day defibrotide intravenously for 7 days and then 400 mg/day intramuscularly for another 20 days. t-PA antigen assessed before and after venous occlusion was not affected by the treatment. Tissue PAI activity significantly decreased and t-PA activity, measured after venous occlusion, increased after 8 and 28 days of treatment; both these changes disappeared after defibrotide was discontinued. No particular side effects were detected throughout the investigation. The study suggests that defibrotide increases t-PA activity by reducing PAI activity.
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PMID:Inhibition of tissue plasminogen activator inhibitor by defibrotide in atherosclerotic patients. 250 72

The changes in coagulation and fibrinolysis were investigated in 10 patients undergoing orthotopic liver transplantation (OLT) which is known to be frequently associated with perturbations of haemostasis. The coagulation profile, already deteriorated before surgery in most patients, showed no appreciable further alteration. On the other hand, important modifications of fibrinolytic parameters occurred, essentially concerning tissue-type plasminogen activator (t-PA) and its specific inhibitor (PAI). t-PA activity constantly increased in the course of transplantation, reaching a maximum at the end of anhepaty. Large interindividual variations were noted in the level of t-PA activity (7.5 to 135 IU/ml). Free PAI activity followed a reverse kinetics, remaining low during the anhepatic stage, and dramatically increasing after allograft reperfusion. Despite the fibrinolytic potential related to high circulating t-PA levels, no biologic nor clinical evidence of systemic fibrinolysis was observed peroperatively. These findings suggest that PAI release could represent an early process making the use of antifibrinolytic drugs during OLT unnecessary.
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PMID:Intraoperative evolution of coagulation parameters and t-PA/PAI balance in orthotopic liver transplantation. 250 68

The aim of this study was to evaluate the existence of an additive effect between standard heparin and dDAVP in the enhancement of endogenous fibrinolysis. Eight healthy volunteers were studied in a randomized double blind placebo controlled cross-over trial. The volunteers were treated i.v. with dDAVP, 0.4 micrograms/kg, over 15 minutes followed by an i.v. bolus dose of either standard heparin, 5,000 I.U., or saline. A 48 hour wash-out period was adopted. The infusion of dDAVP followed by standard heparin resulted in a higher increase in plasma t-PA activity, t-PA antigen, circulating t-PA specific activity and FPLA when compared with dDAVP followed by saline. The difference was already statistically significant at 15 minutes after the infusion of dDAVP and lasted for up to 60 minutes after the end of the infusion of dDAVP. Plasma PAI 1 showed a slightly higher decrease after dDAVP plus standard heparin than after dDAVP plus saline but this difference was not statistically significant. No statistically significant changes of fibrinogen and alpha 2-antiplasmin levels were observed. As expected, the infusion of standard heparin resulted in an increase in plasma anti-Xa activity and in a prolongation of aPTT. Our results demonstrated an additive effect of dDAVP and standard heparin on the increase in circulating t-PA, the effect of dDAVP being potentiated and prolonged by heparin. This observation could prospect a combined use of dDAVP and standard heparin in the prophylaxis and treatment of thromboembolic diseases.
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PMID:Additive effect of dDAVP and standard heparin in increasing plasma t-PA. 185 Aug 74

A 67-year-old man had an acute myocardial infarction with thrombosis in the left anterior descending artery shortly after normal exercise. We were able to measure the fibrinolytic components in this patient just prior to his developing acute myocardial infarction as well as during convalescence. In this case, marked increase in total plasminogen activator inhibitor-1 (PAI-1) antigen, mainly due to free PAI-1 antigen, was observed in basal conditions before the onset of acute myocardial infarction. On the appearance of ischaemia, plasminogen activator activity was suppressed, probably due to decreased tissue plasminogen activator antigen release and increased PAI activity, compared with that during convalescence. This suggests that some patients with coronary artery disease who have a high level of free PAI-1 antigen in basal conditions may have a strong tendency to develop acute myocardial infarction, due to further impaired fibrinolysis on the induction of ischaemia.
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PMID:The role of the fibrinolytic system in acute myocardial infarction after a normal exercise test. 251 1

Blood collected in different anticoagulant/antiplatelet agents (ETP, EDTA, citrate, citrate/citric acid pH 4.5 and CTAD) was compared with respect to determination of PAI-1 activity and PAI-1 antigen. beta TG and PF4 were analysed as markers of platelet release. Both the middle layer and the remaining layer of the plasma were studied. Moreover vWF:Ag, FVII:Ag, ECLT, t-PA:Ag, t-PA activity, APTT, VIII:C and VII:C were assayed in blood collected in citrate and CTAD. PAI-1 activity showed the same level in all citrate based anticoagulants and ETP and no increase was found in blood standing for 2 hours at room temperature. On the contrary quick handling was most important for determination of PAI-1 antigen. In tubes anticoagulated with citrate no significant increase was found if the sample was prepared within 1 hour. EDTA was not suitable as anticoagulant mixture. Tubes containing the antiplatelet mixture CTAD could be used for determination of PAI activity, PAI antigen, vWF:Ag, FVII:Ag, t-PA activity and APTT. For measurement of PAI-1 antigen quick handling of blood anticoagulated with antiplatelet mixtures are preferable, and plasma treated in that manner could also be used to assay some hemostasis parameters.
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PMID:The effect of various anticoagulant/antiplatelet mixtures on determination of plasminogen activator inhibitor, platelet proteins and hemostasis parameters. 252 63

We compared urokinase-type plasminogen activator (u-PA) in fluid phase and u-PA bound with its receptor on human blood monocytes with respect to proteolytic activity and susceptibility to inactivation by the plasminogen activator inhibitors PAI-1 and PAI-2. Receptor-bound u-PA is catalytically twice as efficient as fluid-phase u-PA. Fluid-phase u-PA is susceptible to rapid inhibition by PAI-1 and PAI-2 at an estimated PAI:u-PA molar ratio of 2:1. In contrast, u-PA bound to endogenously occupied receptors is inhibited by PAI-2 only at PAI:u-PA molar ratios of 20:1, but is not inhibited by PAI-1, u-PA/PAI-1 and u-PA/PAI-2 complexes bind to the receptor with a tenfold lower affinity than u-PA itself. Thus, competition of u-PA/PAI complexes with fluid-phase u-PA for binding to the receptor is unlikely to affect the overall plasminogen activator activity of the monocyte. These findings demonstrate that the activity of receptor-bound u-PA can be modulated by PAI-2, but not by PAI-1, to adjust the cell's proteolytic activity to different local situations.
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PMID:Functional characteristics of receptor-bound urokinase on human monocytes: catalytic efficiency and susceptibility to inactivation by plasminogen activator inhibitors. 254 40

Recent studies on circadian variation of blood fibrinolytic activity have suggested a relation between a depressed morning fibrinolytic activity and the frequent onset of myocardial infarction at that time in Caucasians. We have obtained blood samples from 10 Eskimos with an interval of 4 h during 24 h and studied the extrinsic tissue-type plasminogen activator-related fibrinolysis. We observed a significant change in the activity of tissue-type plasminogen activator (t-PA; p less than 0.01) and in the activity of plasminogen activator inhibitor (PAI; p less than 0.001) during 24 h. The activity of t-PA increased more rapidly and the activity of PAI decreased more rapidly during the morning hours in Eskimos compared to reported patterns in Caucasians. A significant negative correlation between PAI and t-PA (r = -0.79, p less than 0.0001) suggested that PAI contributes to the regulation of t-PA activity in the blood. Whether the observations are of importance for the low prevalence of myocardial infarction in Eskimos remains to be further studied. However, our observations demonstrate that it is of utmost importance to standardize the collection of blood samples in order to obtain reliable information on the fibrinolytic system in Eskimos.
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PMID:Circadian variation of fibrinolytic activity among Eskimos in Greenland. 259 Mar 19

Plasminogen activators initiate the fibrinolytic system by conversion of the proenzyme plasminogen to the active fibrin degrading enzyme plasmin. Plasminogen activator inhibitors inhibit the effects of both plasminogen activators. Uncomplicated pregnancies are accompanied by hypercoagulability and an increased risk of thromboembolic disease. Thrombosis is rare in the first trimester and most events are noted in the last trimester. Therefore, we studied the fibrinolytic system at the end of pregnancy and in the puerperium. Plasma concentrations of urokinase plasminogen activator (u-PA/competitive radioimmunoassay), tissue type plasminogen activator (t-PA/sandwich ELISA) and plasminogen activator inhibitor (PAI/functional assay) were determined in 44 women (age: 24.3 +/- 4.3 years) with normal pregnancy near term. Plasma samples were collected before the onset of labour and 1, 2, 3, 4 and 5 days after delivery. Compared with an age-matched non pregnant control group (8.3 +/- 3.94 U/ml) significantly increased PAI activity (12.13 +/- 4.79 U/ml - p less than 0.005) was measured before delivery with a subsequent significant decrease (8.13 +/- 1.97 U/ml) to normal values on day 1 after delivery; plasma u-PA and t-PA antigen levels remained unchanged. Placental weight and birth weight had no influence on plasma levels of both plasminogen activators.
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PMID:Influence of delivery on plasminogen activator inhibitor activity. 268 64


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