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)

We studied a Spanish family in which one of the female members presented recurrent thrombophlebitis in both legs after three different deliveries. Biological and antigenic activity of protein C was decreased (35% and 42% respectively). Reduced protein C levels were also observed in 6 other family members. Administration of danazol (600 mg/day) in two patients with protein C deficiency elevated this protein and discontinuation of the drug resulted in a reduction of protein C to pretreatment values. The proposita showed a normal fibrinolytic activity and infusion of DDAVP produced a similar response of FVIII/VWF and plasminogen activator to those observed in healthy subjects.
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PMID:Protein C deficiency--response to danazol and DDAVP. 384 Feb 87

The aim of the study was to investigate the long-term chronic effects of smoking on the fibrinolytic enzyme system by comparing two groups of healthy male volunteers (aged 30 to 40 years). One group consisted of 15 habitual smokers who consumed 20 or more cigarettes a day; the other consisted of 15 nonsmokers. Fibrinolysis was studied at rest (baseline) and after infusion of 1-desamino-8-D-arginine vasopressin (DDAVP; 0.4 micrograms/kg body weight). Smokers had significantly lower baseline blood fibrinolytic activity as determined by the overall assays: dilute blood clot lysis (p less than or equal to 0.05) and euglobulin-fibrin plate assay (p less than or equal to 0.05). Further analysis showed that these low activities could be attributed to a lower baseline level of extrinsic tissue-type plasminogen activator (t-PA) activity (p less than or equal to 0.05) in the smokers. There were no significant differences between the groups in various fibrinolytic inhibitors or in the intrinsic fibrinolytic activation pathways. The increased levels of t-PA activity and factor VIII R:Ag in response to DDAVP were also reduced in the smokers (p less than or equal to 0.01). The relative increase (ratio of post-DDAVP activity/baseline activity) for these parameters was not significantly different for the two groups. Smokers also had significantly higher levels of the acute phase reactants, alpha 1-antitrypsin (p less than or equal to 0.02) and plasminogen (p less than or equal to 0.02) and C-reactive protein (p less than or equal to 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of chronic smoking on fibrinolysis. 387 92

Although etiology of thrombosis is multifactoral, the single common defect in the majority of case is the deficiency of plasminogen activators in the fibrinolytic defense system. Development of a new immunoradiometric method for determining blood/tissue activators prompted an examination of plasminogen activator blood levels in patients with previously verifed thrombosis. After immunoradiometric testing of plasma of 26 confirmed thrombosis patients, according to the detailed procedure described, and comparing the results with plasma levels of a control group before and after response to venous occlusion, infusion of DDAVP, or exercise, no significant differences were seen between levels in thrombosis patients and controls; increase of plasminogen activator activity was most pronounced in the controls after venous occlusion. The method has shown that 3 stimuli cause an increase in plasminogen activator levels. This is in agreement with previous observations, i.e., that these stimuli increase fibrinolytic activity in the blood. These results do not indicate, however, which of the tests is most suitable for detecting predissposition to thrombosis in certain patients. In order to clarify this point, tests of patients with recurring thromboses must be conducted. Furthermore, this method would not appear to be suitable as a screening process for women taking oral contraceptives to determine possible thrombosis tendency due to the excessive expense involved.
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PMID:[Immunoradiometric determination of blood/tissue plasminogen activators in thrombophilia]. 608 13

Infusion of 0,4 micrograms DDAVP/kg for 30 min increased the plasminogen activator activity in blood of experimental animals (dog, rat, rabbit). The plasminogen activator releasing effect was also demonstrated in isolated perfused vascular preparations (pig ear, rat lung) at low doses (10(-9) - 10(6) mol/l). According to these results DDAVP is believed to attack directly the endothelial cell.
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PMID:[Experimental studies of the liberation of plasminogen activator by DDAVP]. 608 28

Fibrinolytic factors were measured before and after DDAVP-infusion in 18 patients on chronic, regular haemodialysis, 11 of whom underwent bilateral nephrectomy, and in 7 patients in whom non-functioning kidneys were still present. Baseline fibrinolytic activity was normal or high in all but two cases. Before haemodialysis, the response to DDAVP-infusion was greatly reduced in the majority of patients as compared with healthy controls, irrespective of the baseline level. This was in accordance with mean t-PA-antigen levels which increased only slightly after DDAVP. When DDAVP was given after haemodialysis, previous non-responders showed a normal increase in fibrinolytic activity. The level of free t-PA-inhibitors was normal in most cases as were levels of alpha 2-antiplasmin and alpha 2-macroglobulin.
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PMID:Fibrinolytic activators and inhibitors in terminal renal insufficiency and in anephric patients. 608 94

A portion of human blood fibrinolytic activity can be quenched by antibodies to urokinase. We attempted to identify this portion and its position in the three pathways (extrinsic, intrinsic factor XII dependent, and intrinsic factor XII independent) of plasminogen activator activity that have been defined in the DEFs of plasma. Activity quenching in various plasmas (including plasma adsorbed by agarose-bound AUK) demonstrated the involvement of a discrete activator activity of 40 to 50 BAU/ml with little variation among individuals (43 +/- 6 (SD) BAU/ml, n = 13). The quenching did not involve, quantitatively or qualitatively, the extrinsic (tissue-type) plasminogen activator activity varying between 1 and 146 BAU/ml in baseline plasma and in plasma obtained after stimulation by venous occlusion, exercise, or DDAVP administration. In confirmation, extrinsic activator activity was recovered in plasma adsorbed by agarose-bound AUK. The quenching also did not involve the factor XII-dependent activities; it was quantitatively normal in plasma with Hageman (n = 3) and Fletcher (n = 2) traits, and AUK did not interfere with the generation of factor XII-dependent fibrinolytic activity by addition of purified activated factor XII in plasma with Hageman trait. There was no effect of AUK on kallikrein generation, kallikrein activities, or the APPT, nor were these aspects altered in depleted plasma. In conclusion, the quenching involved the factor XII-independent system of intrinsic fibrinolysis. Addition of purified urinary urokinase did not result in restoration of missing activity in plasma adsorbed by AUK-agarose. The quenching, therefore, probably involved an apparent urokinase-related activator component in plasma.
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PMID:Intrinsic plasma fibrinolysis: involvement of urokinase-related activity in the factor XII-independent plasminogen proactivator pathway. 619 46

Functional assay of extrinsic (tissue-type) plasminogen activator (EPA) in plasma on fibrin plates was evaluated. Using specific quenching antibodies, we demonstrated the method to be specific for EPA under all conditions tested. Contributions of urokinases and intrinsic activators were excluded. The quantity of EPA in blood samples, as compared with purified uterine tissue activator, shows 1 blood activator unit (BAU) to be comparable to 0.93 ng. The median values for EPA activity for healthy volunteers were: baseline, 1.9 BAU/ml (n = 123); diurnal, 5.5 BAU/ml (n = 12); DDAVP administration, 11.7 BAU/ml (n = 39); exhaustive exercise, 25 BAU/ml (n = 24); venous occlusion (15 min), 35 BAU/ml (n = 61). A large inter-individual variation in EPA activity was found, while individual baseline values tended to be constant for periods of weeks. In vitro in blood EPA activity shows a disappearance of 50% in about 90 min at 37 degrees C; EPA activity in euglobulin fractions is stable for less than or equal to 2 hr at 37 degrees C. A rapid decrease in EPA activity occurs in vivo, as noted after extracorporal circulation and exercise stimulation (t1/2 decay, 2-5 min).
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PMID:Behaviour and quantitation of extrinsic (tissue-type) plasminogen activator in human blood. 635 52

The effect of DDAVP on blood coagulation factors was investigated after its intravenous infusion into normal subjects. A marked increase in factor XII was observed in addition to the expected rise of factor VIII coagulant activity (VIII:C), factor VIII related antigen (VIIIR:Ag) and plasminogen activator, DDAVP also produced a concomitant but less pronounced rise of factor VII, but there was no change in factors V, IX, X and XI.
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PMID:Effect of DDAVP on plasma level of factor XII. 640 13

In a group of six normal male volunteers, infusion of DDAVP, venous occlusion and exercise were shown to increase plasma levels of factor VIII and plasminogen activator, activity and antigen, to different extents and at differing rates. Any mechanisms suggested to explain release of these proteins by various stimuli should account for such differences. All three stimuli could also increase plasma levels of prostacyclin metabolites, although this was only significant for high doses of DDAVP. Other potential endothelial markers, such as fibronectin and thrombospondin, showed no specific increase after any of the stimuli.
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PMID:A comparative study using immunological and biological assay of the haemostatic responses to DDAVP infusion venous occlusion and exercise in normal men. 642 76

We tested the response of the fibrinolytic activity and factor VIII-antigen levels to infusion of DDAVP in healthy volunteers and we studied the influence of propranolol and aspirin on this response. After DDAVP, 0.4 microgram/kg in 10 min i.v., the fibrinolytic activity of redissolved euglobulins rose from 179 to 452 mm2 (lysis area of fibrin plates); after pretreatment with propranolol, 320 mg per day during 7 days, DDAVP induced a similar rise (from 166 to 471 mm2) and after pretreatment with a single dose of aspirin, 600 mg, ingested 5 hr before the DDAVP infusion, the lysis area increased from 159 to 455 mm2. Factor VIII-antigen level increased within 60 min after DDAVP from 104 to 208%; after pretreatment with propranolol from 111 to 230% and after a single dose of aspirin, DDAVP induced a rise from 107 to 206%. From these data we conclude that neither baseline levels nor the release of plasminogen activator or factor VIII after DDAVP infusion are influenced by beta-blockade or by interference with prostaglandin synthesis.
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PMID:The inability of propranolol and aspirin to inhibit the response of fibrinolytic activity and factor VIII-antigen to infusion of DDAVP. 642 80


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