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

---

Query: EC:3.4.21.6 (thromboplastin)
13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood rheology and several haemostatic factors were studied in patients with type II hyperlipoproteinaemia (HLP) and matched controls. HLP patients had increased blood viscosity (p less than 0.01), the mean level being 18% higher at a low shear-rate (0.94 s-1) and 13% higher at a high shear-rate (94 s-1). The increased viscosity was due partly to a raised haematocrit (p less than 0.05), and partly to increased plasma viscosity (p less than 0.01) associated with increased plasma fibrinogen (p less than 0.02). Red cell deformability was normal, and viscosity was unrelated to either lipid or lipoprotein concentrations. Levels of the major fibrinolytic inhibitor. alpha 2-antiplasmin, measured by both functional and immunological techniques were higher in HLP patients (mean increase 30-32%). Plasminogen activator levels were normal in HLP patients and the ratio of fibrinolytic inhibitor to activator was therefore increased. Plasminogen concentrations were also increased. Levels of factor VIII activity and antigen, antithrombin III and anti-factor Xa activity, alpha 2-macroglobulin, platelet count, and platelet aggregation by adenosine diphosphate and adrenaline did not differ significantly in HLP patients and controls. These results suggest that the premature arterial disease associated with HLP may be related to increased blood viscosity, which reduces arterial blood flow, and increased alpha 2-antiplasmin, the major inhibitor of fibrinolysis.
...
PMID:Increased blood viscosity and fibrinolytic inhibitor in type II hyperlipoproteinaemia. 612 Nov 40

Coagulation and fibrinolysis profiles of naturally menopausal women receiving conjugated estrogens (0.625 or 1.25 mg for 21 of 28 days) and medroxyprogesterone acetate (10 mg for seven of 28 days) for 18 months were compared with those of similar women receiving no hormone therapy. Tests indicative of the dynamics of the coagulation cascade, ongoing intravascular coagulation, and anticoagulation were performed. Hormone therapy had no effect on prothrombin times, activated partial thromboplastin times, or thrombin times. There was no evidence of intravascular coagulation in any of the groups as assessed by platelet counts, fibrinogen antigen and activity, and fibrin degradation products. Antithrombin III antigen and activity, alpha 1-antitrypsin antigen, and alpha 2-macroglobulin antigen, the natural inhibitors of coagulation, were also unaffected by hormone therapy. Plasminogen antigen levels were unaffected, but plasminogen activity was enhanced in the hormone-treated groups, suggesting a stimulatory effect on fibrinolysis. These data indicate that in terms of the coagulation system, healthy women can safely use a combined regimen of conjugated estrogens and medroxyprogesterone acetate.
...
PMID:Combination estrogen and progestogen replacement therapy does not adversely affect coagulation. 662 49

The fibrinolytic response to trauma was investigated in 23 patients. Patients were triaged upon arrival in the emergency center into three groups; group I-patients with significant trauma who maintained normal vital signs, had a good prognosis, and tolerated the trauma well (mean injury severity score 8, range 4 to 12); group II--patients with significant trauma and transient episodes of hypotension, hypoxia, or acidosis who recovered (mean injury severity score 22, range 9 to 38); and group III--patients with profound or continued hypoxia and hypotension who eventually died of the trauma (mean injury severity score 41, range 30 to 50). Serial measurements of prothrombin time, activated partial thromboplastin time, and platelet count; concentrations of fibrinogen, plasminogen, and fibrin degradation products; and assays of euglobulin fraction fibrinolytic activity on plasminogen-free and plasminogen-rich fibrin plates were obtained on all patients. Coagulation studies documented a trauma-related coagulopathy that correlated with the degree of trauma. Plasminogen concentrations were initially depressed in all three groups; however by 24 hours group III patients were noted to have significantly elevated plasminogen concentrations while group I and group II patients had normal plasminogen concentrations. Fibrinolytic activity measured on plasminogen-free and plasminogen-rich fibrin plates was initially increased in all three groups with group III patients demonstrating the greatest increase. Over the succeeding 14 hours fibrinolytic activity returned to baseline values in group I and group II patients while group III patients demonstrated no detectable fibrinolytic activity for the remainder of the study period. This absence of fibrinolytic activity and increase in plasminogen concentrations in group III patients is thought to be caused by depletion of the intravascular plasminogen activator with the subsequent development of a hypofibrinolytic state.
...
PMID:Fibrinolytic response to trauma. 671 Mar 42

Serial coagulation studies were obtained in 25 patients treated with intracoronary streptokinase infusion for myocardial infarction (23 patients) or coronary insufficiency (two patients) to determine the frequency of systemic fibrinolytic activity. Clotting studies were obtained before and after infusion and at 4-hour intervals until normalization. Intracoronary thrombolysis was successful in 20 of 23 patients (87%) with myocardial infarction. Streptokinase dosage in this study was 201,000 +/- 74,000 IU (+/- SD). Systemic fibrinolytic activity, defined as greater than 70% reduction of fibrinogen using a functional assay (Claus method), occurred in 22 of 25 patients (88%) and was present at a mean streptokinase dosage of 119,000 +/- 52,000 IU. Fibrinogen in the total population decreased from 342 +/- 80 to 87 +/- 94 mg% (p less than 0.0001). In patients with systemic effect, the mean fibrinogen level after infusion was 17% of baseline, increased to 43% at 24 hours, and returned to normal at 30 hours. Plasminogen decreased to 7% of baseline activity after infusion (p less than 0.0001), was 44% of baseline at 24 hours, and returned to normal at 48 hours. Intraprocedural sampling during infusion showed reduction of fibrinogen by 25% after 30,000 IU (p less than 0.0005) and by 71% at 120,000 IU (p less than 0.0001); plasminogen decreased by 50% after 30,000 IU (p less than 0.0001) and by 84% at 120,000 IU (p less than 0.0001). Prothrombin time increased from 11.5 +/- 0.8 seconds to 22.0 +/- 7.8 seconds after infusion (p less than 0.0001) and returned to normal at a mean of 18 +/- 11 hours after infusion. Partial thromboplastin time was markedly prolonged (greater than 100 seconds) after infusion, returned to less than or equal to 2 times control at 5 +/- 2 hours, and returned to normal at 9 +/- 4 hours after infusion. Fibrinogen degradation products were less than 10 micrograms/ml before infusion, increased to greater than 40 micrograms/ml after infusion, and remained greater than 40 micrograms/ml in 40% of patients at 24 hours after infusion. These data indicate that systemic fibrinolytic activity occurs in a high percentage of patients with "low-dose" intracoronary streptokinase infusion and that coagulation variables may be altered for 24-48 hours after infusion.
...
PMID:Fibrinolytic effects of intracoronary streptokinase administration in patients with acute myocardial infarction and coronary insufficiency. 683 67

The relationship between gastric mucosal hemorrhage and coagulation-fibrinolysis of fasting, restraint and water immersion stress (FS) rats was studied in comparison with normal (N) and fasting (F) rats. In this case, the FS group was fasted for 18 h prior to the stress application and then subjected to restraint and water immersion for various intervals. The F group was fasted for 18 h plus the time comparable to the stress load. Gastric mucosal erosions with bleeding were recognized from 1 h after the stress load only in FS group and the hemorrhagic erosion index progressively increased 1 to 16 h. In the FS group, prothrombin time and active partial thromboplastin time gradually prolonged with time course from 8 and 1 h, respectively, and plasma prothrombin level remarkably decreased from 1 h, although no changes in these parameters were observed in the F group. Plasminogen activator activity in gastric mucosa significantly increased in not only FS group but also F group from 0.5 h as compared with N group. However, no significant difference was seen between F and FS groups on this activity. Plasma plasminogen and antiplasmin levels in FS group were lower than those of N group, 3 h later. It is suggested from these results that sustained hemorrhage from the gastric mucosa in this stress ulcer may be associated with high fibrinolytic activity in the gastric mucosa and the delay of blood coagulation.
...
PMID:Biochemical studies on experimental stress ulcer. I. Gastric mucosal hemorrhage and coagulation fibrinolysis in rat stress ulcer. 697 25

Screening coagulation tests, coagulation factors, and components of fibrinolysis and kinin generation were examined in 21 healthy adult cats. Observed ranges for screening tests were: prothrombin time, 7.3 to 11.4 s; activated partial thromboplastin time, 10.6 to 14.9 s; and thrombin time, 10.7 to 18.9 s. Functional coagulation factors II, V, VII, VIII, IX, X, XI, and XII were assayed and expressed as percentage of normal. Although individual factors varied, the observed range for factors assayed was 37% to 208% of normal. Fibrinogen ranged from 50 to 165 mg/dl. Plasminogen and antithrombin III ranged from 50% to 200% and 89% to 111% of normal, respectively. Plasma kallikrein ranged from 0.3 to 3.9 mukat/L. Fibrin(ogen) degradation products and fibrin monomers were examined with variable and inconsistent results.
...
PMID:Coagulation, fibrinolysis, and kinin generation in adult cats. 710 32

Components of the coagulation and fibrinolytic cascades, prothrombin and activated partial thromboplastin times, endotoxin activity, and albumin concentration were measured in blood and peritoneal fluid from 20 healthy horses and from 153 horses with acute gastrointestinal tract diseases at admission. Overall, 77% (117/153) of affected horses survived to discharge from the hospital, and 85% (82/97) of horses discharged were reported to be normal 9 to 14 months later. Significant differences in hemostatic factors were more common in peritoneal fluid than in blood. Tissue plasminogen activator, plasminogen, protein C, antithrombin III, and alpha 2-antiplasmin activities and concentrations of fibrinogen and fibrin degradation products were significantly (P < 0.05) greater in peritoneal fluid from horses with colic, and, with the exception of fibrinogen concentration, were associated with detection of endotoxin. Higher values for these variables, except tissue plasminogen activator activity, were significantly (P < 0.05) associated with survival. Plasminogen, antithrombin III, and alpha 2-antiplasmin activities were significantly (P < 0.05) greater in peritoneal fluid from horses with inflammatory or strangulating lesions, compared with those in horses with simple colic. Plasminogen-activator inhibitor type 1 activity, fibrin degradation products concentration, and prothrombin time were significantly (P < 0.05) greater in the blood of horses with colic. Survival was inversely associated with significantly (P < 0.05) greater intravascular concentrations of fibrin degradation products and fibrinogen and prothrombin time. This study revealed marked contrasts between peritoneal and intravascular coagulation and fibrinolysis in horses with colic, indicating that inferences regarding the peritoneal environment, particularly with respect to fibrinolytic capacity, should not be made on the basis of factors measured in blood.
...
PMID:Intravascular and peritoneal coagulation and fibrinolysis in horses with acute gastrointestinal tract diseases. 759 47

Plasminogen activator has been isolated from the culture of pig kidney cells by gel-filtration on Sephadex G-75. The plasminogen activator (181.9 MU/200 g body weight) protected the animals against thrombosis hazard in case of provocation by thromboplastin and exerted a thrombolytic effect in case of thrombus appearance.
...
PMID:[The antithrombotic and thrombolytic activity of a plasminogen activator isolated from a monolayer cell culture]. 785 66

Plasminogen activator inhibitor type 1 (PAI-1), a member of serine proteinase inhibitor superfamily, is known to inhibit thrombin in the presence of either heparin or vitronectin. We analyzed possible inhibitory activity of PAI-1 on human factor Xa. PAI-1 inhibited factor Xa in the presence of calcium ion (Ca2+), whereas no inhibition was observed in the absence of Ca2+. Half maximal enhancement by Ca2+ was obtained at 0.8 mM. An equimolar complex formation between factor Xa and PAI-1 in the presence of Ca2+ was observed by SDS polyacrylamide gel electrophoresis. Both unfractionated heparin and vitronectin enhanced the inhibition only in the presence of Ca2+. Apparent second-order rate constant (ki) for the inhibition of factor Xa by PAI-1 at 5 mM Ca2+ was 1.6 x 10(4) M-1 s-1, and was enhanced 3-fold by 2 u/ml of heparin (4.6 x 10(4) M-1 s-1) and 10-fold by 100 nM vitronectin (1.6 x 10(5) M-1 s-1), respectively. The interaction between Ca(2+)-bound factor Xa and PAI-1 could be important from the view of PAI-1 neutralization and enhancement of fibrinolysis.
...
PMID:The inhibition of human factor Xa by plasminogen activator inhibitor type 1 in the presence of calcium ion, and its enhancement by heparin and vitronectin. 898 Jun 46

Plasminogen has been immobilized onto a segmented polyurethane containing amino groups, using glutaraldehyde as coupling agent. It was also aspecifically adsorbed, for sake of comparison, onto polyurethane films containing different functional groups and, in particular, epsilon-amino caproic acid and lysine residues. The differently immobilized plasminogen has been converted to plasmin by activation with urokinase, and the percentage of active plasmin for the various polymer films was determined using a tripeptide (S-2251) as a synthetic substrate. The biological behaviour of the differently treated polymer films has been evaluated in vitro by measurements of partial thromboplastin time (PTT) and platelet adhesion.
...
PMID:Preparation and evaluation of polyurethane surfaces containing immobilized plasminogen. 904 Oct 39


<< Previous 1 2 3 4 5 Next >>

---