Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.4.21.7 (plasmin)
9,023 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We assayed plasma concentrations of fibrinogen, fibrinopeptide A, plasmin-alpha 2 plasmin inhibitor complex, D dimer, and antithrombin III activity in 40 patients with cerebral thrombosis and nine patients with cerebral embolism during the acute (less than 7 days), subacute (7-27 days), and chronic (greater than or equal to 28 days) periods and compared these with 69 controls. In cerebral thrombosis, fibrinogen and fibrinopeptide A levels were elevated significantly in all stages (p less than 0.001), whereas plasmin-alpha 2 plasmin inhibitor complex and D dimer levels were elevated significantly in the subacute and chronic periods. The antithrombin III activity was significantly decreased in the acute stage. The elevation of fibrinogen and plasmin-alpha 2 plasmin inhibitor complex levels in the acute stage was significantly greater in patients with an infarct size greater than 10 mm2 compared to patients with an infarct size less than 10 mm2. We observed similar changes in patients with cerebral embolism. These results suggest that enhanced coagulation exists at all stages and endogenous fibrinolysis is activated in the subacute and chronic periods in a large proportion of patients with cerebral thrombosis and embolism.
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PMID:Coagulation-fibrinolysis abnormalities in acute and chronic phases of cerebral thrombosis and embolism. 214 32

Activation of hemostasis during surgery was investigated in 30 elective cases, who underwent either gastric (group G) or hepatic (group H) resection by a serial determination of various molecular markers such as fibrinopeptide A (FPA), fibrinopeptide B beta 15-42 (B beta 15-42) D-dimer, thrombin-antithrombin III complex (TAT) and plasmin-alpha 2 plasmin inhibitor complex (PIC). In both groups, the values of FPA and TAT were significantly elevated intraoperatively, indicating an occurrence of hypercoagulable state. The degree of the elevation was more marked in group H, probably due to greater tissue damage during hepatic resection. Also in both groups, the values B beta 15-42 and PIC were significantly increased during surgery, while the amount of D-dimer was within normal range in most cases, indicating the occurrence of the primary fibrinolysis. These findings are compatible with our previous observations on the postoperative changes in hemostasis. There were statistically significant but variable correlations between the values of fibrinopeptides and the enzyme-inhibitor complexes. The absolute values of the molecular markers of fibrinolysis were always higher than those of coagulation, suggesting that a considerable amount of plasmin, rather than thrombin, is released by surgical tissue damages.
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PMID:Activation of coagulation and fibrinolysis during surgery, analyzed by molecular markers. 214 15

Prothrombin complex concentrates (PCC), licensed for the treatment of hemophilia B, are known to carry a significant risk of thromboembolic complications. Although the reasons for thrombogenicity are not completely understood, several manufacturers have developed purified factor IX concentrates that contain negligible amounts of the other vitamin K-dependent factors. To evaluate whether or not the infusion of such a factor IX concentrate is followed by lesser activation of the hemostatic system than by the infusion of a PCC, we performed a series of coagulation assays on 11 hemophilia B patients before and after the administration of these two types of concentrate using a randomized cross-over design. The levels of prothrombin fragment F1 + 2, a sensitive measure of the in vivo cleavage of prothrombin by factor Xa, was significantly increased in plasma after PCC, but not after factor IX concentrate. Plasma fibrinopeptide A, a sensitive index of the enzymatic activity of thrombin on fibrinogen, also increased significantly after PCC but not after factor IX concentrate. The fragment B beta 15-42, a sensitive index of the enzymatic action of plasmin on fibrin II, did not change after either concentrate. There were also no differences in less sensitive coagulation measurements, such as plasma fibrinogen, antithrombin III, and fibrin monomers, nor in indices of platelet activation, such as beta-thromboglobulin and platelet factor 4. These findings show that the infusion of a purified factor IX concentrate can result in substantially less activation of the coagulation cascade than may be seen with PCC.
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PMID:Thrombin generation is not increased in the blood of hemophilia B patients after the infusion of a purified factor IX concentrate. 226 48

The coagulability of plasmas from 63 patients with acute ischemic stroke (cerebral thrombosis and cerebral embolism) was analyzed by an automated method for prothrombin time using a fluorogenic peptide substrate. The fluorogenic prothrombin time (FPT) of patients' plasmas collected within 48 hr after onset, as expressed as percent of control plasma, was significantly higher in cerebral thrombosis than in an age-matched control group (p less than 0.01). The high values of FPT in cerebral thrombosis patients were observed until the 30th day after onset. On the other hand, FPT values in cerebral embolism patients were not significantly different than that of the control group. Factor VII activity levels in cerebral thrombosis patients were significantly higher than those of the control group and cerebral embolism patients, while levels of factor X activity were not significantly different among these groups. Although FPT and factor VII activity in these stroke patients did not significantly correlate, factor VII activity did correlate well with factor VII antigen. Decreased levels of antithrombin III and elevated levels of FDP and alpha 2-antiplasmin-plasmin complexes were observed only in cerebral embolism patients. Our findings strongly suggest that patients with cerebral thrombosis have been in a hypercoagulable state before the onset of symptoms, which was caused in part by an increase of factor VII activity/antigen, and in part by other unknown mechanisms. In contrast, patients with cerebral embolism were in a low grade consumptive coagulopathy.
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PMID:Hypercoagulability in acute ischemic stroke: analysis of the extrinsic coagulation reactions in plasma by a highly sensitive automated method. 236 33

In order to assess precisely the fibrinolytic state in disseminated intravascular coagulation (DIC), plasma levels of fibrinogenolysis products (FgDP), fibrinolysis products (FbDP) and fibrinogenolysis plus fibrinolysis products (TDP) were measured with newly developed enzyme-linked immunosorbent assays based on monoclonal antibodies in 72 patients with DIC at presentation. Not only FbDP and TDP but also FgDP were markedly elevated in patients with DIC. When analyzed according to the underlying disease categories, the relative proportion of FgDP to TDP was high in patients with acute promyelocytic leukemia and vascular diseases, and it was the lowest in patients with sepsis. Correlation analysis revealed that plasma levels of FgDP correlated negatively with alpha 2-antiplasmin and positively with plasmin-alpha 2-antiplasmin complex (PAP) and a ratio of PAP to thrombin-antithrombin III complex (TAT). These findings indicate that besides fibrinolysis, fibrinogenolysis is markedly accelerated in the majority of the patients with DIC.
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PMID:Fibrinolysis and fibrinogenolysis in disseminated intravascular coagulation. 240 38

Physical exercise causes shortening of activated partial thromboplastin time (aPTT) and euglobulin clot lysis time. To investigate whether this activation of coagulation and fibrinolysis leads to in vivo thrombin or plasmin action after long distance running, 19 well trained male runners (36-65 years) were examined 5 to 53 min after termination of a 100 km race and 5 days later after at least 1 day without physical exercise. Compared to the control examination aPTT was decreased (30.2 +/- 2.8 vs 35.3 +/- 3.0 sec) and the following parameters were increased after the race: beta thromboglobulin (40 +/- 16 vs 23 +/- 7 ng/ml), thrombin-antithrombin III (TAT) complexes (5.5 +/- 3.4 vs 2.3 +/- 0.7 microgram/l), the fibrin(ogen) degradation products fragment E (57 +/- 15 vs 35 +/- 7 ng/ml) and B beta 15-42 (8.5 +/- 2.5 vs 6.5 +/- 2.5 ng/ml) (all p values less than 0.001). Platelet count, platelet factor 4, fibrinoepetide A (FPA) and haematocrit did not change significantly. Increased TAT complexes and unchanged FPA suggest that the generated thrombin was fully inactivated by antithrombin III (AT III) and did therefore not give rise to fibrin formation. The small increase of fibrin(ogen) degradation products indicates a minor in vivo activity of the fibrinolytic system. This investigation demonstrates the importance of AT III in the regulation of haemostasis in activated blood coagulation.
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PMID:Blood coagulation after long distance running: antithrombin III prevents fibrin formation. 240 46

125I-labelled alpha 2-macroglobulin complexed with thrombin or plasmin bound to hepatocytes in a concentration- and time-dependent manner. The apparent Kd values calculated from displacement experiments were 7.9 X 10(-8) M for alpha 2-macroglobulin-thrombin and 8.5 X 10(-8) M for alpha 2-macroglobulin-plasmin. Association of these complexes was only partially reversible; after a 180 min incubation period, 50-60% of the bound radioactivity was internalized by the cells. alpha 2-Macroglobulin itself bound also to hepatocytes, but the affinity of the alpha 2-macroglobulin complexes was higher than that of the inhibitor alone, and alpha 2-macroglobulin was not internalized, either. 125I-labelled thrombin or plasmin bound to hepatocytes as well. These bindings were also concentration-dependent and could be decreased with an excess of unlabelled ligands. Binding rates and amounts of the bound proteinases were higher than those of their alpha 2-macroglobulin complexes. The alpha 2-macroglobulin-thrombin complex competed with the alpha 2-macroglobulin-plasmin complex in binding to hepatocytes, whereas there was no competition between these complexes and the antithrombin III-thrombin complex. These results suggest that the binding sites of hepatocytes for alpha 2-macroglobulin-proteinase and antithrombin III-proteinase complexes are different.
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PMID:Association of alpha 2-macroglobulin-thrombin and alpha 2-macroglobulin-plasmin complexes with isolated hepatocytes. 240 76

Severe rejection crises occurred in 13 out of 20 cadaver kidney recipients; removal of the graft was inevitable in 10 cases. The plasminogen levels were found to be lower (76.5 +/- 2.9%) in the 13 patients with impaired graft acceptance (group B) than in the 7 patients experiencing only moderate rejection (group A, 93.7 +/- 5.2%, p less than 0.01) or the 41 patients with chronic renal disease (group C, 88.2 +/- 2.3%, p less than 0.01). Since alpha 2-antiplasmin was found to be enhanced, the alpha 2-antiplasmin/plasminogen ratio was high (1.56 +/- 0.07) in group B as compared with group A (1.19 +/- 0.05, p less than 0.002) and group C (1.11 +/- 0.04, p less than 0.001). The fibrinolytic capacity, which was assessed by a "reversed fibrin plate" assay, declined significantly after transplantation, and was lower in group B greater than 20 days after grafting. The neoantigen alpha 2-antiplasmin-plasmin complex was not detected in any patient; thus hyperfibrinolysis is unlikely to be responsible for the plasminogen decrease. Protein C rose above preoperative values (group A 117.1 +/- 8.7%; group B 133.7 +/- 9.0%) and reached higher levels in group A (221 +/- 24.1%) than in group B (157.4 +/- 14.8%, p less than 0.05) between days 11 and 20 after transplantation. No constant alterations were found with respect to antithrombin III and fibrinogen. Fibrin deposits, which reduce perfusion, can be found in the vessels of rejected kidney grafts. An impaired fibrinolytic capacity and a subsequent inability to remove these clots may be significant for the outcome of transplantation.
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PMID:Impaired fibrinolysis and protein C increase after cadaver kidney transplantation. 242 20

Isolated human basilar arteries were used in this study to evaluate the inhibitory effect of antithrombin III (AT III), thrombin, and alpha 2-macroglobulin (alpha 2-M) on contractions elicited by K+, serotonin (5-HT), prostaglandin (PG) D2, PGF2 alpha, and plasmin. alpha 2-M (0.5-1.0 mg/ml) failed to affect the contractions produced by contractile agonists significantly but did notably reduce the basal tone of the arteries. Thrombin (1 and 10 U/ml) reduced basal tone and significantly inhibited the contractions elicited by K+, PGF2 alpha, and plasmin. The relaxant effect of thrombin was abolished by procedures that destroy endothelium and by exposing the artery to thrombin for prolonged periods (tachyphylaxis). AT III (1-6 U/ml) reduced basal tone and significantly inhibited, in a concentration-dependent manner, the contractile responses to K+, 5-HT, PGD2, PGF2 alpha, and plasmin. In sharp contrast to thrombin, AT III did not induce tachyphylaxis nor was its vasorelaxant effect significantly reduced by destruction of the endothelium. The results show AT III to be a potent and nonspecific inhibitor of human cerebral arteries and support the hypothesis that AT III may contribute to the delay of cerebral vasospasm seen in patients who experience aneurysmal hemorrhage.
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PMID:Comparison of the inhibitory effects of antithrombin III, alpha 2-macroglobulin, and thrombin in human basilar arteries: relevance to cerebral vasospasm. 243 98

Oxidative inactivation of alpha-1-proteinase inhibitor (A1-P1) and plasminogen activator inhibitor-1 (PAI-1), both members of the serine protease inhibitor (serpin) superfamily, using mild oxidation conditions has been already demonstrated. The oxidation mechanism has been shown to involve conversion of methionine to methionine sulfoxide in the reactive center of the inhibitors. In this study evidence is presented that alpha-2-antiplasmin (A2-PI) and antithrombin III (AT III) can also be inactivated by means of oxidation. For total inactivation of 50 pM A1-PI about 10 nM chloramine T (CT) and for the same molar concentration of A2-PI and AT III about 250 nM CT were found necessary. C1-inhibitor (C1-INH) showed some resistance to oxidation that could be overcome only by increasing CT to an amount (greater than 2000 nM) already beginning to inactivate the corresponding C1-esterase. As target enzymes for A2-PI, AT III, and A1-PI plasmin, thrombin and elastase, respectively, were used. Their activity was not impaired by the oxidation conditions applied. As there is no methionine in the reactive center of AT III an additional mechanism for oxidative inactivation of serpins has to be taken into consideration. Oxidation seems to be a general mechanism for altering the balances between serine proteases and their inhibitors in favour of the protease.
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PMID:Oxidative inactivation of purified human alpha-2-antiplasmin, antithrombin III, and C1-inhibitor. 245 61


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