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)

Plasma fibrinopeptide A, thrombin-antithrombin III complexes, tissue-plasminogen activator and alpha 2-plasmin inhibitor-plasmin complexes were measured early in the first stage of labor, in the second stage of labor and at 15 min after placental separation. Fibrinopeptide A and thrombin-antithrombin III complex levels did not change from the first to the second stage of labor but increased significantly after placental separation. There was a significant increase of the tissue-plasminogen activator level between the early first stage of labor and the second stage of labor, and it remained high after placental separation. A significant increase in the level of plasma alpha 2-plasmin inhibitor-plasmin complexes was observed after placental separation. These findings suggest that activation of the thrombotic system occurs at the time of placental separation and that activation of the fibrinolytic system begins during labor before placental separation to compensate for the hypercoagulable state which develops at the time of delivery.
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PMID:The influence of labor on thrombotic and fibrinolytic systems. 153 54

In 11 healthy young subjects, the plasma concentrations of the thrombin-antithrombin III complex, fibrinopeptide A, tissue-plasminogen activator, complement fragments C3a and C4a, and histamine were measured before and after a graded maximal bicycle exercise test. The analyses were carried out 30 min before and immediately before exercise, immediately after exercise, and 30 and 60 min later. All post-exercise values were corrected for plasma volume changes, which were calculated from hematocrit and hemoglobin values. Immediately post-exercise, thrombin-antithrombin III, tissue-plasminogen activator, complement fragments C3a and C4a, and histamine were all significantly elevated (p less than 0.01), compared with the pre-exercise values; 30 and 60 min later the values normalized and significant differences from the pre-exercise values could no longer be measured. Fibrinopeptide A did not change significantly after exercise. The present results provide evidence for a simultaneous activation of coagulation, fibrinolysis, and complement system as well as for a release of histamine after a short maximal exercise.
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PMID:Effect of a short maximal physical exercise on coagulation, fibrinolysis, and complement system. 171 17

The development of hemodialysis treatment has remarkably improved the prognosis of chronic hemodialysis (HD) patients. However, as the patient's survival time is prolonged, vascular damages due to the abnormalities of calcium and lipid metabolism and hypertension has become the important complications in HD patients. In addition to coagulation and fibrinolysis, vascular endothelial function has been pursued to clarify the pathogenesis for occurrence of thrombosis in HD patients with more than ten years' duration. Twenty-two HD patients including twelve of less than ten years' duration and ten of more than ten years' were subjected to this study. Twelve healthy controls were also involved in this study. Fibrinopeptide A (FPA) and thrombin-antithrombin III complex (TAT) as indexes of coagulation, antithrombin III (AT III) as an index of coagulation inhibitor and D-dimer as an index of fibrinolysis were measured. A special attention has been focused in changes in the levels of tissue plasminogen activator (t-PA) activity and antigen and plasminogen activator inhibitor-1 (PAI-1) as indexes of fibrinolysis capacity, representing parameters of vascular endothelial functions. Levels of FPA, TAT and D-dimer were significantly higher in HD patients when compared with those in healthy controls. In particular, levels of FPA were significantly higher in HD patients with more than ten years' duration as compared to those in HD patients with less than ten years'. AT III values were significantly lower in HD patients with more than ten years' duration than those in healthy controls. T-PA activity and antigen levels were significantly lower in HD patients than those in healthy controls. T-PA activity levels were lower in HD patients with more than ten years' duration than those in HD patients with less than ten years'. Among HD patients, a significant negative correlation was found between t-PA activity and hemodialysis duration. PAI-1 values in HD patients were not significantly differ from those in healthy controls. These results suggest that in spite of increased coagulability, fibrinolytic capacity of vascular endothelium decreased in HD patients, and that the incidence is accelerated as hemodialysis duration is prolonged. Therefore, it is concluded that long-term HD patients are in the state of a higher risk of thrombosis.
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PMID:[Long-term hemodialysis and changes in variables of coagulation and fibrinolysis]. 177 13

Fibrinopeptide A (FPA) is a very sensitive marker of fibrin generation in vivo. Because an imbalance between thrombogenic and thrombolytic forces may be responsible for the failure to recanalize and for reocclusion of coronary arteries, such a marker could be of eminent value during thrombolytic treatment of acute myocardial infarction. Thirty-four consecutive patients with acute myocardial infarction (peak creatine kinase level, 1,869 +/- 1,543 IU/l) were treated with 100 mg recombinant tissue-type plasminogen activator (rt-PA) 3.1 +/- 1.1 hours after onset of chest pain. Angiography 12.5 +/- 6.1 days later revealed an 81% patency rate of the infarct-related vessel. FPA plasma levels (normal, 1.9 +/- 0.5 ng/ml) were 34 +/- 46 ng/ml on admission and 93 +/- 86 ng/ml (538 +/- 674% with respect to each patient's admission level) after 90 minutes of rt-PA infusion (p less than 0.01). In patients without evidence of reocclusion (including three primary failures), FPA levels fell under continuous heparin infusion to 6.7 +/- 9.7 ng/ml (24 +/- 33%, p less than 0.01) within 30 minutes and were 3.1 +/- 2.2 ng/ml (15 +/- 15%, p less than 0.01), 1.6 +/- 1.1 ng/ml (8 +/- 10%, p less than 0.01), and 2.5 +/- 3.0 ng/ml (12 +/- 16%, p less than 0.01) 30 minutes, 9 hours, and 21 hours, respectively, after completion of rt-PA therapy. Five patients sustained intermittent or permanent coronary reocclusion after primary thrombolytic success. Their early postlytic FPA levels (13-51 ng/ml) remained high or increased again despite adequate anticoagulation. FPA allows the monitoring of fibrin generation during acute myocardial infarction and thrombolytic therapy. Despite successful recanalization, fibrin generation is increased under rt-PA administration before anticoagulation. Patients under anticoagulation with postlytic FPA levels less than 5 ng/ml or below their admission value seem to be at low risk of reocclusion for several days. FPA levels that are persistently high or that increase again despite adequate anticoagulation indicate ongoing fibrin generation. However, whether FPA can indeed be considered a useful marker of reocclusion remains to be confirmed in a larger population of patients with acute myocardial infarction.
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PMID:Monitoring of fibrin generation during thrombolytic therapy of acute myocardial infarction with recombinant tissue-type plasminogen activator. 249 39

The effect of heparin as an anticoagulant was examined and the extent of fibrinolytic activity during cardiopulmonary bypass (CPB) was measured. Twenty patients undergoing valve replacement or aortocoronary bypass surgery were studied. Fibrinopeptide A (FPA) levels gradually became elevated as CPB proceeded, and antithrombin III (AT III) decreased during CPB. This indicates that despite the use of heparin, the coagulation system was activated, leading to fibrin formation in the microcirculation. On the other hand, fibrinopeptide B (FPB beta 15-42) also increased to four times the preoperative value at two hours on CPB. Intrinsic fibrinolytic activity, as determined by the activity of kaolin-activated euglobulin, was transiently increased only at the beginning of CPB. The C1 inactivator-resistant fibrinolytic activity and tissue plasminogen activator antigen (t-PA;Ag) increased sharply during CPB and reached maximum levels one hour after the start of CPB, indicating that enhanced fibrinolytic activity during CPB is predominantly of extrinsic origin as the result of t-PA release from the vascular walls. It is concluded from the above findings that thrombin activity continues during CPB. Enhanced fibrinolytic activity during CPB appears to be important because t-PA activates plasminogen predominantly where fibrin is formed, leading to dissolution of the microthrombi formed during CPB.
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PMID:Alterations in coagulation and fibrinolysis associated with cardiopulmonary bypass during open heart surgery. 253 75

Fibrin formation and fibrinolysis were estimated in 89 breast cancer patients by measurement in plasma of Fibrin Fragment B beta 15-42 and Fibrinopeptide A (FPA), serum Fibrin(ogen) Degradation Products (FDPs) and plasminogen activator by Fibrin Plate Lysis Assay. Results were compared with (a) 26 patients with benign breast diseases; and (b) 45 healthy factory workers. FPA, FDP and B beta 15-42 levels were elevated in both breast cancer patients and benign disease patients, but there were no significant differences between these two groups. Cancer stage, patient age and smoking habits did not affect these results, but Oestrogen Receptor (ER) positive patients had higher B beta 15-42 values than ER negative patients (p = 0.017). These results show that fibrin formation is enhanced preoperatively in patients with either benign or malignant breast disease. The fibrinolytic response to activated coagulation may be relatively deficient in breast cancer. The roles of malignancy, stress and other factors in the causation of these abnormalities require further assessment.
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PMID:In vivo measurements of fibrin formation and fibrinolysis in operable breast cancer. 281 34

To investigate the effect of blood glucose concentration on thrombin generation and fibrinolytic activity, six Type 1 patients had the blood glucose concentration maintained for 1 h at 5, 15, and 25 mmol l-1, and 8 patients underwent hypoglycaemia of 20 min duration after the blood glucose had been kept at 8 mmol l-1 for 1 h. During hyperglycaemia plasminogen activator activity rose from 214 (11-625) (median, range) to 478 (18-772) units (p less than 0.05) at a blood glucose of 5 mmol l-1 and to 511 (89-816) (p less than 0.05) and 535 (33-976) (p less than 0.05) units at a blood glucose of 15 and 25 mmol l-1, respectively. Cross-linked fibrin degradation products (FDP) were 45 and 53 micrograms l-1 at a blood glucose of 5 mmol l-1 and remained unchanged at higher glucose levels. Fibrinopeptide A was 1.3 (0.6-2.8) nmol l-1 at a blood glucose of 5 mmol l-1, and remained unchanged with hyperglycaemia, being 1.3 (0.9-1.3) nmol l-1 after 1h at 25 mmol l-1. During hypoglycaemia, plasminogen activator activity rose from 155 to 745 units (p less than 0.05) while both fibrinopeptide A and cross-linked FDP remained unchanged. The results indicate that acute fluctuations in blood glucose concentration do not lead to thrombin generation. Additionally, increased fibrinolytic activity measured in vitro is not associated with an increase in cross-linked FDP. This suggests that short-term hyper- and hypoglycaemia do not affect the end-products of the coagulation and fibrinolytic pathways.
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PMID:Acute changes in blood glucose concentration do not promote thrombin generation or fibrin breakdown in type 1 diabetes. 297 49

Plasma concentrations of vasopressin (aVP) attained under conditions of stress were simulated by infusing four volunteers with 0.25, 0.5, 1.0 and 2.0 pressor units of aVP over 1 h (units/h). Three subjects had all four infusions and one received only 1.0 unit/h. Blood samples were taken for assay of factor VIII coagulant activity (FVIIIC), factor VIII related antigen (FVIIIRAg), the ristocetin cofactor (FVIIIRiCof), euglobulin lysis time (ELT) and aVP concentrations before infusion (time 0) and every 20 min for 80 min. Fibrinopeptide A (FPA) generation time was measured at time 0, 60 and 80 min. At infusion rates of 0.25 unit/h median aVP levels peaked at 6.5 pg/ml and there was no change in FVIII or FPA generation time, and plasminogen activator activity (10(6)/ELT2) rose from 100 to 400 units. At 1.0 unit/h, aVP levels rose to 25.4 pg/ml, FVIIIC rose by 160% and activator activity from 87 to 360 units. At 2.0 units/h, aVP concentrations reached 83 pg/ml, there was an increase in all modalities of FVIII and activator activity rose from 251 to 452 units. FPA generation time shortened and circulating plasma levels of FPA were increased. There was a highly significant correlation between the percentage increases in all three components of FVIII and plasma aVP levels (FVIIIC: r = 0.87, P less than 0.0001; FVIIIRAg: r = 0.61, P less than 0.0001; FVIIIRiCof: r = 0.80, P less than 0.0001) and between the increase in plasminogen activator activity and aVP levels (r = 0.56, P less than 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of physiological concentrations of vasopressin on haemostatic function in man. 393 Jan 28

Green pit viper (Trimeresurus albolabris and Trimeresurus macrops) venom was found to have a thrombin-like effect in vitro but cause a defibrination syndrome in vivo. The effects of venom on fibrinolytic system have not been well characterized. This knowledge can help to define the roles of antifibrinolytic therapy, give insights in fibrinolytic system regulation and potentially lead to identification of a new profibrinolytic agent from this venom. Forty-six cases of green pit viper bites were studied for various coagulation and fibrinolytic parameters and correlated with serum venom levels measured by ELISA. Fibrinolytic system activation is very common as indicated by low plasminogen (50%), low antiplasmin (56.5%) and elevated fibrin-fibrinogen degradation products (FDPs, 97.4%) levels. FDP test is very sensitive and a normal level is useful for exclusion of systemic envenomation. In contrast to some other models of defibrination syndrome, such as Russell viper (Daboia russelli siamensis), elevation of plasminogen activator activity (PA) was found indicating a hyperfibrinolytic state. Definite increase in tissue-type plasminogen activator (t-PA) antigen (p = 0.00075) with a modest elevation of its inhibitor plasminogen activator inhibitor-1 (PAI-1) (p = 0.27) probably contributes to this effect. This supports the idea that the balance between plasminogen activators and inhibitors can determine fibrinolytic responses in pathologic states. Fibrinopeptide A levels were markedly elevated (68.43 +/- 51.57 ng/ml in cases and 2.83 +/- 3.80 ng/ml in control, p < 0.0001) and correlated well with clinical severity suggesting that the fibrin deposition from the thrombin-like effect is the main mechanism of fibrinolysis. Therefore, antifibrinolytic agents probably have no role in treatment. However, the components of green pit viper venom that have these profibrinolytic effects in human are interesting and should be further identified.
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PMID:The effects of green pit viper (Trimeresurus albolabris and Trimeresurus macrops) venom on the fibrinolytic system in human. 1021 86

Bronchoalveolar lavage fluids (BALF) from patients with hypersensitivity pneumonitis (HP; n = 35), idiopathic pulmonary fibrosis (IPF, n = 41) and sarcoidosis (SARC, n = 48) were investigated for alterations in the alveolar hemostatic balance. Healthy individuals (n = 21) served as Controls. Procoagulant activity (PCA), tissue factor (TF) activity and F VII activity were assessed by means of specific recalcification assays. The overall fibrinolytic activity (FA) was measured using the (125)I-labeled fibrin plate assay. Fibrinopeptide A (FP-A), D-Dimer, plasminogen activators (PA) of the urokinase (u-PA) or tissue type (t-PA), PA-inhibitor I (PAI-1) and alpha2-antiplasmin (alpha2-AP) were determined by ELISA technique. As compared to Controls, all groups with interstitial lung disease (ILD) displayed an increase in BALF PCA by approximately one order of magnitude, and this was ascribed to enhanced TF activity by >98%. Accordingly, F VII-activity was increased in all ILD groups, and elevated FP-A levels were noted. There was no significant difference in procoagulant activities between the different ILD entities, but the increase in TF was significantly correlated with deterioration of lung compliance. Overall fibrinolytic activity did not significantly differ between ILD entities and Controls, although some reduction in IPF subjects was observed. Nevertheless, changes in the profile of the different pro- and antifibrinolytic compounds were noted. U-PA, but not t-PA levels were significantly reduced in all ILD groups. alpha2-AP was markedly elevated throughout, whereas PAI-1 levels were lowered. As a balance of
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PMID:Enhanced tissue factor pathway activity and fibrin turnover in the alveolar compartment of patients with interstitial lung disease. 1089 38


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