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)

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 this report, we investigated the expression and activation of proteolytic enzymes by mouse T-lymphoma cell lines of differing metastatic potential. In contrast to the low metastatic Eb line, the metastatic variants ESb and ESb-MP secreted urokinase-type plasminogen activator (u-PA), which was present in the culture supernatant predominantly in the active form (ESb, 96%; ESb-MP, 80%). All three T-lymphoma variants expressed a mainly cell surface-associated proteinase, which proved to be immunologically and enzymatically related to the murine T-cell-associated serine proteinase-1 (MTSP-1). Intact lymphoma cells were able to activate the recombinant human proenzyme of u-PA (pro-u-PA) by a plasmin-independent mechanism, because plasmin contamination of the cells was not detectable. When ESb-MP cells were cultured in the presence of inhibitors of MTSP-1, such as antithrombin III, Pro-Phe-Arg-chloromethylketone, or aprotinin, the ratio of endogenously activated murine u-PA to inactive pro-u-PA in conditioned medium was significantly reduced (from 80% to 15%). The most potent inhibitor, antithrombin, did not inhibit plasmin-catalyzed pro-u-PA activation. These results suggest a novel autocrine mechanism of plasmin-independent pro-u-PA activation for metastatic T lymphomas by the production of an MTSP-1-related proteinase. The ability to initiate the proteolytic cascade of plasminogen activation in the absence of plasmin might contribute to the metastatic behavior of these cells observed in vivo.
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PMID:A T-cell-related proteinase expressed by T-lymphoma cells activates their endogenous pro-urokinase. 156 36

The effects of physical training on hemostatic parameters were evaluated in 56 postmyocardial infarction (MI) patients before and after one month of systematic physical training and in 30 control post-MI patients, who did not undergo such training. There were no significant changes in prothrombin time (PT) and alpha 1-antitrypsin (alpha 1AT) at the beginning and end of the study in either group. Levels of fibrinogen, Factor VIII: C (VIII:C) and von Wildebrand antigen (vWf:Ag), and activities of ATIII and plasminogen (Plg) were significantly decreased in the group with physical training (p less than 0.05), while values were unchanged in the control group. Hematocrit, platelet counts, and alpha 2-plasmin inhibitor (alpha 2PI) activities also decreased in the physical training group (p less than 0.05). In contrast, these variables increased in the control group (p less than 0.05). Activated partial thromboplastin time (aPTT) tended to be prolonged in the group with physical training, while it was shortened in the control group. In a subset of 20 patients with physical training, resting levels of plasmin-alpha 2PI complex (PIC), thrombin-antithrombin III complex (TAT), protein-C (P-C:Ag), plasminogen activator inhibitor-1 (PAI-1), VII:C, and P-C activities had significantly decreased after one month of physical training (p less than 0.05), although tissue plasminogen activator activities remained unchanged. Physical training appeared to suppress coagulability as indicated by the decrease in fibrinogen, VIII:C, vWf:Ag, VII:C, and TAT, and prolongation of aPTT. The decrease in plasminogen, t-PA:Ag, alpha 2PI, PAI-1, and PIC after physical training may result from the decreased coagulability. In conclusion, physical training appears to induce a suppression of the coagulation system in patients in the recovery phase of MI.
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PMID:Blood coagulability and fibrinolytic activity before and after physical training during the recovery phase of acute myocardial infarction. 162 56

The changes in coagulation and fibrinolysis were studied in cases of hepatocellular carcinoma with (n = 20) and without (n = 8) transcatheter hepatic arterial embolization (TAE). The plasma levels of thrombin-antithrombin III complex (TAT) and alpha 2 plasmin inhibitor complex (PIC) were significantly elevated after TAE, concurrently with a decrease in antithrombin III and antiplasmin (alpha 2-plasmin inhibitor) levels. The elevation of TAT was most significant (2.4-fold of the pre-TAE level) on day 3, whereas that of PIC was relatively less (1.3-fold on day 3). Tissue plasminogen activator in blood was also significantly increased on day 1, but it was decreased thereafter, although plasminogen activator inhibitor (PAI) remained high for at least 7 days after TAE. In contrast, such hematological changes were not observed in patients without TAE. Thus, both coagulation and fibrinolysis were activated after TAE, but its effect on fibrinolysis was less prominent, due probably to the increased synthesis of PAI.
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PMID:Effects of transcatheter hepatic arterial embolization on coagulation and fibrinolysis in patients with hepatocellular carcinoma. 166 Feb 19

A study was made of blood coagulation, physiological anticoagulants and fibrinolysis in 120 elderly patients with cerebrovascular diseases, including 50 subjects in the acute period of ischemic brain stroke. To estimate activation of the fibrinolytic system, the levels of plasminogen and free plasmin were measured. Phasic changes in the system of blood coagulation were detected, variants of antithrombin III depression were delineated, and a relationship was established between the activity of enzymes of the fibrinolytic system and the site of an ischemic focus in the brain. Five coagulopathic syndromes of the acute period of brain stroke were distinguished, the principles of their differentiated treatment were based.
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PMID:[Diagnosis and treatment of coagulopathic syndromes in ischemic stroke]. 166 74

Release of tissue plasminogen activator (t-PA) and its interaction with plasma protease inhibitors were studied in two patients with massive defibrination, one after electroshock and soft tissue injury and the other after complicated labor; both had very severe hemorrhage. Large quantities of free t-PA were present in the circulation for several hours. Complexes of t-PA with plasminogen activator inhibitor 1 (PAI-1), alpha 2-macroglobulin and C1-inhibitor were also observed. PAI-1 antigen rose dramatically in both patients, and complexes of t-PA with PAI-1 rose rapidly during the period of observation. In contrast, the complexes of t-PA with alpha 2-macroglobulin and C1-inhibitor, present initially, persisted for short periods only and disappeared when free t-PA disappeared from the circulation. Plasmin was generated initially, as indicated by the presence of plasmin-alpha 2-antiplasmin complexes. Plasma concentrations of alpha 2-macroglobulin, C1-inhibitor, antithrombin III, and alpha 2-antiplasmin were severely depleted initially, but rapidly returned to normal. The observations demonstrate that there is a major release of t-PA in such defibrinating patients, that there is a role for protease inhibitors other than PAI-1 in the regulation of endogenous t-PA, and indicate the great rapidity with which such free t-PA is complexed and cleared.
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PMID:Complexing of tissue plasminogen activator with PAI-1, alpha 2-macroglobulin, and C1-inhibitor: studies in patients with defibrination and a fibrinolytic state after electroshock or complicated labor. 168 22

In order to assess the thrombin and plasmin generation in vivo in disseminated intravascular coagulation (DIC), plasma levels of thrombin-antithrombin III (ATIII) complex (TAT) and plasmin-alpha 2-antiplasmin (a2AP) complex (PAP) were measured together with standard coagulation and fibrinolytic parameters in 80 patients with DIC. Both TAT and PAP were markedly elevated in patients with DIC. When plotted by the underlying disease categories, differences in the magnitude of the elevations of these complexes were recognized among groups. Patients with acute promyelocytic leukemia (APL) had the highest PAP, the lowest TAT/PAP ratio, low a2AP, and low fibrinogen, indicating that the most excessive fibrinolysis can occur in APL. Similar profiles, although less marked, were observed in patients with other leukemias and vascular diseases. Patients with sepsis showed the highest TAT/PAP ratio and the lowest PAP with no decrease in a2AP or fibrinogen, demonstrating a relatively impaired fibrinolysis. Patients with cancer had a relatively high TAT and high TAT/PAP ratio. In addition, both TAT and PAP were markedly elevated in patients with shock. From these, it was suggested that, although laboratory manifestations in DIC are extremely variable from patient to patient, underlying disorders are, at least in part, responsible for the observed variations. Recognition of this variable activation of coagulation and fibrinolysis would be helpful for the proper management of patients with DIC.
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PMID:Thrombin vs. plasmin generation in disseminated intravascular coagulation associated with various underlying disorders. 200 32

Severe bleeding took place in a patient when abdominal aneurysm was removed by operation. Bleeding continued after infusion of heparin, antithrombin III (ATIII), fresh platelets and fresh blood. Infusion of tranexamic acid resulted in an immediate cessation of bleeding and improvement of his general condition. Sometime after the cessation by the administration of tranexamic acid, severe bleeding started again, resulting in intraperitoneal hematoma formation. Second time bleeding also stopped after the administration of tranexamic acid. Major finding of plasma parameters of fibrinolysis is that alpha 2AP which had been unable to inhibit plasmin, became able to inhibit it after the administration of tranexamic acid.
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PMID:Prevention of severe bleeding by tranexamic acid in a patient with disseminated intravascular coagulation. 169 50

The aim of this study was to evaluate the balance between thrombin and plasmin activity in a group of 79 diabetic patients (IDDM and NIDDM). For this purpose we determined fibrinopeptide A (FPA) and B beta 15-42, specific products of thrombin and plasmin activity. Moreover we investigated the behaviour of antithrombin III and alpha 2 antiplasmin, important inhibitors of blood coagulation and fibrinolysis. Results show an increase both in FPA and B beta 15-42 in IDDM and NIDDM patients when compared to healthy controls. However the ratio between B beta 15-42 and FPA was lower than in controls indicating an imbalance between thrombin and plasmin activity. Antithrombin III levels were not different from the controls and no correlation was found with Hb A1c. alpha 2 antiplasmin was found to be higher in IDDM when compared both with NIDDM and controls. A non linear correlation was found between Hb A1c and alpha 2 AP in both diabetic groups. We conclude that the imbalance between thrombin and plasmin activity may have a role in determining fibrin deposition. These subclinical abnormalities, unrelated to vascular complications and duration of the disease, may progressively contribute to the development of the vascular complications in diabetes.
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PMID:Is the imbalance between thrombin and plasmin activity in diabetes related to the behaviour of antiplasmin activity? 169 51

The regulation of plasmin, miniplasmin, and streptokinase-plasmin complex (SkPm) was studied in vitro in the presence of unfractionated porcine intestinal heparin using purified plasma proteinase inhibitors. Heparin enhanced the reaction of antithrombin III (AT) with plasmin (up to 40-fold with 20 units/ml). The rate of plasmin inhibition by alpha 2-antiplasmin (alpha 2AP) and by alpha 2-macroglobulin (alpha 2M) was not changed by heparin (0.5-100 units/ml); the rank-order of plasmin-inhibitory activity remained alpha 2AP greater than alpha 2M greater than AT. The reaction of miniplasmin with AT was studied also. The second order rate constant was 9.2 x 10(2) M-1s-1 without heparin and 2.6 x 10(4) M-1s-1 in the presence of 20 units/ml heparin. Heparin did not affect the rank-order of miniplasmin-inhibitory activity; it remained alpha 2M greater than alpha 2AP greater than AT. While the reaction of AT with SkPm was negligible, heparin stimulated this reaction dramatically. The SkPm-inhibitory activity of alpha 2AP was not changed by heparin. When plasma concentrations of alpha 2AP (1.05 microM) and AT (4.76 microM) were compared, AT inhibited greater amounts of SkPm in the presence of more than 5 units/ml of heparin. The increased SkPm-inhibitory activity of AT in heparin did not result from SkPm dissociation, and heparin did not decrease the rapid rate of streptokinase association with plasmin. These studies demonstrate that heparin can affect the regulation of fibrinolysis at multiple levels of the enzyme cascade.
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PMID:Regulation of plasmin, miniplasmin, and streptokinase-plasmin complex by alpha 2-antiplasmin, alpha 2-macroglobulin, and antithrombin III in the presence of heparin. 170 Apr 88


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