Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.68 (tissue plasminogen activator)
 11,311 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of invasive investigations on parameters of hemostasis and fibrinolysis is generally unknown, although this has consequences for the design of prospective studies on the association between those parameters and regression or progression of atherosclerosis. We therefore determined hemostatic and fibrinolytic factors in 12 patients who were admitted to the hospital for coronary angiography (CAG; n = 5) or percutaneous transluminal coronary angioplasty (PTCA; n = 7). Blood samples were drawn under basal circumstances on the day before, the day of and the day after CAG or PTCA. Significant changes occur in the concentrations of platelets and white blood cells, hematocrit (Ht), von Willebrand factor antigen (vWF:ag), antithrombin III-activity (AT III-ag), antithrombin III-antigen (AT III-ant), fibrinogen, plasminogen, alpha2-antiplasmin (alpha2-AP), histidine-rich glycoprotein (HRG), and plasminogen activator inhibitor (PAI)-activity. Mean values of beta-thromboglobulin, platelet factor 4, factor VIII:C, tissue-type plasminogen activator activity (t-PA act) and euglobulin clot lysis time (ECLT) do not differ significantly. After correction for Ht, no significant differences exist between the day before and the day of the procedure; but on the day after CAG and PTCA significant differences occur in white blood cells, factor VIII:C, AT III-ag, alpha2-AP and PAI-act. It is concluded that principally blood samples for investigations on fibrinolysis may be taken on the day before or the day of CAG or PTCA without a loss of quality, if the values are corrected for Ht. Samples taken on the day after the procedure are not useful for such purposes.
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PMID:The influence of coronary angiography and angioplasty on parameters of hemostasis and fibrinolysis. 214 44

Envenoming by Russell's viper caused a marked rise in FPA, B beta 15-42 fragment and fibrin derived cross-linked D-dimer fragment indicative of a consumptive coagulopathy with hyperfibrinolysis. There was no increase in tPA or tPA-I levels post envenoming, which suggests that the increase in fibrinolytic activity was not due to venom-induced release of tPA from the vessel walls but may have been attributable to a direct effect of the venom or to a secondary physiological response to fibrin deposition. The effectiveness of the antivenom is demonstrated by its ability to prevent further cleavage of fibrinogen and the return to normal fibrinogen levels by 24 h. A secondary rise in FPA at this time indicates that the initial dose of antivenom may have been too small. The antivenom alone or in combination with the venom causes the release of tPA, tPA-I and vWF by the vessel walls. This may be a consequence of the severe anaphylactic reactions seen in some patients.
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PMID:The action of Russell's viper venom on fibrin formation and fibrinolysis in vivo. 249 16

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

Eighty patients undergoing total hip replacement (THR) were randomly allocated to three groups. Group I (n = 29) received general anaesthesia, Group II (n = 29) epidural anaesthesia and Group III (n = 22) the same epidural as Group II and the same general anaesthesia as Group I but with a lower isoflurane concentration. Prothrombin time (PT), activated thromboplastin time (APTT), fibrinogen (FG), plasminogen (PG), antithrombin III (AT III), protein C (Proc C), alpha-2-antiplasmin (alpha 2AP), Factor VIII coagulating activity (F VIII:C), von Willebrand factor antigen (vWF:Ag), von Willebrand ristocetin cofactor (vWF:Rcof), tissue plasminogen activator (tPA) as antigen and activity were measured before induction (A), at the end of surgery (B), on the first postoperative morning (C) and 7 days postoperatively (D). The most relevant finding was that AT III was equally depressed immediately after surgery in all groups, but returned to normal significantly faster in the epidural group (mean values at C: 96.2% in Group I, 104.1% in Group II, 92.7% in Group III). The faster return to normal of AT III after epidural anaesthesia could be one of the mechanisms responsible for the beneficial effect of this technique on the prevention of thromboembolic complications.
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PMID:Coagulation and fibrinolytic parameters in patients undergoing total hip replacement: influence of the anaesthesia technique. 268 46

Haemostatic variables were assessed in 43 patients, 28 insulin-dependent and 15 non insulin-dependent. Maximum aggregation by low concentrations of adenosine diphosphate (ADP) or arachidonic acid and elevated plasma concentrations of TxB2, Factor VIII, vWF:Ag, RCoF and fibronectin (Fnct) indicated a hypercoagulable state. The manifestation of vasculopathy was associated with elevated concentrations of RCoF, Fnct, Hbalc, cholesterol and triglycerides, while impaired fibrinolysis was demonstrated by decreased t-PA levels and the absence of crosslinked fibrin degradation products (XL-FDP).
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PMID:Diabetes mellitus as a hypercoagulable state: its relationship with fibrin fragments and vascular damage. 311 98

The blood loss-reducing effect of desmopressin during dextran therapy was studied in a double-blind fashion in 79 elderly but otherwise healthy patients with preoperative normal bleeding time undergoing total hip replacement for primary coxarthrosis. An infusion of desmopressin (0.3 microgram/kg body weight) or placebo was randomly administered immediately after administration of spinal anaesthesia and six hours later. Haemostasis was evaluated on the basis of vWF: ristocetin cofactor activity, FVIII: C activity, human tissue plasminogen activator (tPA) plasminogen activator inhibitor type (PAI), beta-thromboglobuline (beta TG) and a clot impedance test (Sonoclot). There were no statistically significant differences (P > 0.05) in mean blood loss or transfusion requirements between the placebo and the desmopressin group. There was a significantly increase (P < 0.01) both in vWF: ristocetin cofactor and in FVIII: C activity after both infusions of desmopressin compared with placebo. There was no significant difference in beta TG, tPA, PAI or Sonoclot analysis between the groups. In conclusion, desmopressin did not reduce blood loss in patients undergoing total hip replacement.
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PMID:Desmopressin acetate does not reduce blood loss during total hip replacement in patients receiving dextran. 757 6

Cerebrovascular disease is one of the major causes of morbidity and mortality in the developed world. A number of important risk factors have been identified with the occurrence of stroke, including advancing age, hypertension, smoking and diabetes mellitus, but the mechanisms that link these risk factors to the development of cerebrovascular disease are unclear. The pathogenesis of cerebrovascular disease includes syndromes of atherothrombotic brain infarction and intracerebral hemorrhage. The role of abnormalities of the coagulation and fibrinolytic systems in these processes has not been properly evaluated with regard to clinical outcome, although there is evidence that raised concentrations of fibrinogen are associated with an increased risk of stroke. Smaller studies have identified increases in FVIII/vWF in association with acute stroke and raised levels of tissue plasminogen activator. Although factor VII is considered a risk factor for coronary artery disease, little is known regarding its role in the development of cerebrovascular disease. Improved understanding of the pathogenesis of stroke and the potential to predict patients at risk of stroke should herald the beginning of new approaches in stroke management.
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PMID:Risk factors for cerebrovascular disease and the role of coagulation and fibrinolysis. 757 90

We studied a series of hemostasis factors in a group of patients selected from a cohort of 916 patients affected by MI from the GISSI-2 study population. Following a case-control design, 73 patients with a family history of thrombosis (the presence of at least two first degree relatives affected by MI and/or stroke before 65 years) were matched with MI patients with no family history of thrombosis. Blood collection could be performed 6 +/- 1 months after the acute phase following MI in 53 pairs of such patients. The presence of mixed disulphides (MDS) was significantly higher in patients with family history than in controls; MDS were detected in 7 cases and only in 1 control. No difference was found in contrast in the distribution of fibrinogen, factor VII, factor VIII, vWF, protein C, protein S, AT III, HC II, PAI-1, lipoprotein (a). Nevertheless, independently from the family history, in the whole population of MI patients studied, 21 cases of suspected deficiency of protein C were found. Sixteen out of 53 patients with family history of MI and/or stroke had a family history of MI only. In patients with family history of MI the t-PA antigen levels were significantly lower than in the control group (7.5 +/- 4.4 vs 11.1 +/- 3.5 ng/ml, t = -2.6, p < 0.02). In the whole population of MI patients and in patients with a family history of thrombosis t-PA antigen was positively correlated with PAI-1 antigen and vWF. The correlation with PAI-1 was lost in patients with family history of MI.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Hemostatic factors and family history of thrombosis in patients with a myocardial infarct: a case-control study. The participants in GISSI-2-Efrim. Gruppo Italiano per lo Studio della Streptochinasi nell'Infarto Miocardico]. 764 26

Healthy endothelium is a metabolically active interface between the blood and extravascular tissues. Its intimal surface is anticoagulant and antithrombotic, and it secretes a variety of molecules involved in regulating platelet function and blood coagulation. The rapid interactions between platelets, their secreted components, or thrombin and endothelial cells at sites of vessel damage ensure the local secretion of mediators such as prostacyclin and nitric oxide that limit the intravascular growth of the haemostatic plug. There is considerable evidence that a decreased ability of endothelial cells to synthesize NO contributes to the pathogenesis of arterial disease. Local deficiency of PGI2 synthesis has also been implicated in the thrombotic problems in haemolytic uraemic syndrome. Endothelium is also the source of circulating von Willebrand factor, important for efficient platelet adhesion. Chronically elevated plasma levels of vWF in a series of diseases where there is vascular pathology apparently reflect endothelial cell damage or activation, and may contribute to the prothrombotic tendency they exhibit. They may be compounded by decreased levels of the surface anticoagulant thrombomodulin, if the increased concentrations of the soluble forms of thrombomodulin detected in the circulation under similar conditions are a reflection of loss from the endothelium. Further alterations of function in a procoagulant/prothrombotic direction take place when endothelial cells are exposed to certain cytokines or lipopolysaccharide. Tissue factor synthesis is induced, thrombomodulin expression is decreased, and there is enhanced sensitivity of vWF secretion. In addition, the balance of tissue-type plasminogen activator and plasminogen activator inhibitor type I secretion is changed in favour of the latter. These processes are each likely to contribute to the occurrence of disseminated intravascular coagulation which can accompany septic shock.
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PMID:Endothelial cell function and thrombosis. 784 94

The vascular endothelium plays a pivotal role in regulating the hemostatic system. Various cytokines, such as interleukin-1 (IL-1) and tumor necrosis factor (TNF) are known to perturb endothelial cells to reduce antithrombogenicity. On the other hand, blood flow has been shown to affect the endothelium to maintain its antithrombogenicity under some levels of shear stress in the laminar flow system. We examined the role of hemodynamic forces on the vascular system under cytokine stimulation using a cone-plate type viscometer. Treatment of endothelial cells with either IL-1 beta or TNF-alpha under static conditions increased PAI-1, vWF and prostacyclin release, while t-PA secretion was unchanged. When cells were exposed to steady shear stress of 0, 6, 12, 18 and 24 dyne/cm2, the release of t-PA, t-PA-PAI complex and prostacyclin elevated with the increase of shear stress intensity, while a gradual decrease of total PAI-1 secretion was observed and vWF secretion was unchanged. On the contrary, active PAI-1 secretion was significantly decreased under the shear stress of over 18 dyne/cm2. Interestingly, cytokines, which did not affect t-PA secretion of resting cells, increased the t-PA secretion and had an additive effect on prostacyclin secretion with shear stress under the shear stress of over 18 dyne/cm2. PAI-1 elevation induced by cytokines was markedly abolished under the same shear forces. No additive effect was observed in the secretion of vWF. Thus, shear stress attenuates the alteration of the balance in the fibrinolytic and coagulation system induced by cytokines. These findings clearly indicate that hemodynamic forces play a crucial role in regulating the hemostatic activity in vivo.
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PMID:[Effect of shear stress on hemostatic regulation in endothelium]. 784 84


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