Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The recently developed ELISA for the thrombin-antithrombin III complex (TAT) is a sensitive, specific, and simplified means of detecting intravascular coagulation. For further evaluation of the thrombogenicity of a polyamide (P) and a Hemophan (H) hollow-fibre dialyzer a cross-over study was done in ten stable patients on maintenance hemodialysis. At the same doses of heparin (mean bolus of 30 U/kg bw and maintenance doses of 86 U/kg bw), thrombin time and partial thromboplastin time were significantly lower using H. At the end of dialysis TAT was significantly higher in H (mean +/- SEM before HD 3.57 +/- .56, at 240 min 14.9 +/- 6.5 ng/ml, p less than 0.05, Wilcoxon-test) than in P (before HD 4.36 +/- .98, at 240 min 8.95 +/- 3.0 ng/ml, p less than 0.05 H 240 vs. P 240, Wilcoxon-test). Visible clotting was more pronounced in the H filter. Among other favourable features of blood compatibility the polyamide/polyvinylpyrrolidone copolymer with a hydrophilic/hydrophobic microdomain structure has less thrombogenicity. The modified cellulosic membrane H has advantages in complement activation and leukocyte depression, but thrombogenicity seems less favourable since the incorporated diethyl-amino-ethyl groups with their positive charge bind and inactivate negatively charged heparin.
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PMID:Formation of thrombin-antithrombin III complex using polyamide and hemophan dialyzers. 163 30

We investigated the effect of oral contraceptives with low and high estrogen concentration on blood coagulation and thrombogenesis, induced by vascular subendothelium of rabbit aorta exposed to flowing human blood. Twenty healthy women intending to take oral contraceptives were studied [1] before drug ingestion (control), and subsequently during the intake of oral contraceptives with [2] low estrogen content (20 micrograms ethinyl estradiol and 150 micrograms desogestrel per day) and [3] high estrogen content (50 micrograms ethinyl estradiol and 125 micrograms desogestrel per day). All experiments were performed between day 17 and 21 of the menstrual cycle and drug effects were studied during the third tablet cycle. Deposition of fibrin, platelets and platelet thrombi on vascular subendothelium was tested at a defined blood flow and wall shear rate (10 ml/min, 650 s-1) and was quantified by morphometrical techniques. Treatment with the low and high dose contraceptive increased the plasma levels of ethinyl estradiol (728 +/- 139 and 1438 +/- 212 vs. 0 fmol/l [low and high dose vs. control], means +/- SEM, P less than 0.001) and fibrinogen (2.3 +/- 0.1 and 2.6 +/- 0.1 vs. 2.0 +/- 0.1 g/l, P less than 0.05); and decreased antithrombin III activity (95 +/- 3 and 92 +/- 3 vs. 101 +/- 3 %, P less than 0.05). Fibrin deposition on vascular subendothelium was enhanced by the high dose contraceptive only (47 +/- 4 vs. 35 +/- 4 % coverage of the subendothelial surface with fibrin, high dose vs. control, P less than 0.05). The subendothelial deposition of platelets and platelet thrombi was not changed by contraceptive treatment. These results indicate that treatment with high dose contraceptives leads to an increase of fibrin-subendothelial interactions, whereas low dose contraceptives do not significantly alter the blood-subendothelium interactions. observed in this ex vivo model of thrombogenesis.
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PMID:Effects of low and high dose oral contraceptives on blood coagulation and thrombogenesis induced by vascular subendothelium exposed to flowing human blood. 183 26

Reduced oxygen tension is regarded as the primary physiologic signal for the production of erythropoietin (EPO). There is little information available about early changes of EPO production in man due to severe hypoxia. The purpose of the present study was to examine the time course of EPO in serum of patients with acute cardiogenic pulmonary edema (ACPE). In 29 patients (seventy-five +/- six years, mean age +/- SEM) who were hospitalized within two hours after onset of symptoms of ACPE, serum EPO concentrations were monitored for up to seventy-two hours. At the moment of admission all patients showed significantly increased EPO concentrations of 121 +/- 64 mU/mL (mean +/- SEM) compared with a healthy population (15-35 mU/mL). Twenty-three patients who recovered within thirty minutes (group A) exhibited a quick return of their EPO serum levels to normal. The remaining 6 patients (group B) had a protracted clinical course and their EPO concentration showed a further increase up to the end of the observation period. The comparative monitoring of concentrations of alpha-1-proteinase inhibitor, antithrombin III, C-reactive protein, fibronectin, hapotoglobin, and transerrin in serum and plasma revealed no significant changes. Thus a major contribution of fluid shifts into or from the intravascular compartment to the observed changes in EPO concentration seems to be unlikely. The data suggest that the production and release of EPO in the kidneys due to altered oxygen delivery is a fast-responding mechanism.
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PMID:Serum-erythropoietin concentration during acute cardiogenic pulmonary edema. 201 19

The intraperitoneal fibrin formation and its inhibition by intraperitoneal heparin and/or antithrombin III (AT III) were examined in 8 patients on continuous ambulatory peritoneal dialysis (CAPD). With 1,000 and 2,000 U/L of heparin added to inflow dialysate, the concentration of fibrinopeptide A (FPA) in plasma decreased from 39.43 +/- 5.30 (mean +/- SEM) to 8.00 +/- 2.20 and to 0.74 +/- 0.12 ng/ml, respectively. The FPA concentration in outflow dialysate decreased from 34.20 +/- 5.75 to 12.94 +/- 2.10 ng/ml (1,000 U/l of heparin) and to 4.54 +/- 0.79 ng/mg (2,000 U/l of heparin). The AT III concentration was 0.47 +/- 0.07 mg/dl in dialysate and that in plasma was 24.20 +/- 2.76 mg/dl. With 100 U/bag of AT III added to inflow dialysate, the AT III concentration increased from 0.47 +/- 0.07 to 3.36 +/- 0.17 mg/dl in outflow dialysate but did not increase in plasma. The inhibition of fibrin formation of intraperitoneal heparin was increased by addition of AT III without a systemic inhibitory effect on fibrin formation. These data suggest that intraperitoneal administration of heparin without AT III would be sufficient for the purpose of preventing fibrin formation in CAPD patients without any trouble, and additional AT III might increase inhibitory effect of heparin.
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PMID:Inhibitory effect of heparin and/or antithrombin III on intraperitoneal fibrin formation in continuous ambulatory peritoneal dialysis. 207 97

The influence of a disturbed hemostasis as one of the causes of retinal or ciliary vascular occlusions is still controversial. Antithrombin III, protein C and its cofactor protein S were investigated in 25 patients; 14 of them with a retinal vein occlusion, five showed an occlusion of retinal arteries and six of ciliary arteries. Patients with a preceding thromboembolic disease were excluded from the investigations. The mean values (+/- SEM) of antithrombin III (12.1 IU/ml +/- 0.4), protein C (116% +/- 4), total protein S (102% +/- 3) and free protein S (46% +/- 2) were equivalent to the mean values of a normal population. Neither does a defect or a lack of coagulation inhibitors have an essential influence on the development of an isolated retinal or ciliary vascular occlusion nor does the local occlusive vascular disorder influence the activity of systemic inhibitors.
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PMID:[Inhibitors of blood coagulation in vascular occlusion of the retina and optic nerve]. 214 89

The activity elimination half-life of heat-treated antithrombin III (AT III) concentrate was studied in 5 healthy pregnant and 5 preeclamptic women with a documented AT III deficiency. Healthy pregnant women received 1500 units over 20 minutes. Serial blood specimens were obtained over the next 12 hours. The mean (+/- SEM) activity elimination half-life of AT III was 29.4h +/- 3.4h. Preeclamptic subjects had a mean baseline AT III activity of 70.5 +/- 2% (range 61 to 75%). Their activity eliminator half-life after 3000 units of AT III concentrate was 8.5 +/- 1.2h. There was a direct relationship between the pre-concentrate AT III activity level and the AT III activity elimination half-life (r = 0.79, p = 0.01) for all subjects. Based upon parameters calculated from the first infusion, the AT III activity of preeclamptic subjects was maintained by a constant infusion at approximately 100% for 96h. At the conclusion of the infusion, the activity elimination half-life was again measured. A dramatic increase in the activity elimination half-life was demonstrated (433.6h). We conclude that the activity elimination half-life of AT III concentrate is increased during normal pregnancy and further increased in preeclamptic women with an acquired deficiency.
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PMID:Elimination of antithrombin III concentrate in healthy pregnant and preeclamptic women with an acquired antithrombin III deficiency. 235 44

It is thought that a hypercoagulable state contributes to the pathogenesis of coronary artery disease (CAD), but few sensitive markers have been available for detecting the state. In the present study the plasma level of thrombin-antithrombin III complex (TAT), a specific indicator of thrombin generation in blood, was investigated before and after a submaximal exercise test in 18 patients with CAD and in 12 healthy controls. The mean (+/- SEM) value of plasma TAT before the exercise was 3.30 (0.81) ng/ml in the patient group and 1.49 (0.08) ng/ml in controls, and its level increased to 29.22 (5.74) ng/ml and 12.07 (2.89) ng/ml after the exercise, respectively. Thus, the TAT value in the patient group was higher than that in the controls both before and after the exercise. However, no differences could be found between the groups in the following parameters; prothrombin time, activated partial thromboplastin time, antithrombin III, fibrinogen, FDP, plasminogen, alpha 2-plasmin inhibitor, and alpha 2-macroglobulin. Through these results it was concluded that plasma TAT level could be a sensitive marker for latent activation of blood coagulation, and also that the results of these experiments showed that patients with CAD were in a latent hypercoagulable state.
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PMID:Application of thrombin-antithrombin III complex for detecting a latent hypercoagulable state in patients with coronary artery disease. 269 50

The ascitic form of a chemically-induced pancreatic ductal adenocarcinoma in the Syrian golden hamster was very bloody and indistinguishable from blood macroscopically. Unlike blood, the bloody fluid remained unclotted at room temperature. To explore the possibility of presence of anticoagulants, we mixed 40% cell-free fluid with 60% normal human plasma and tested the clottability of the mixture with standard techniques. Plasma containing the fluid showed markedly prolonged activated partial thromboplastin time (APTT), thrombin time (TT) and recalcification time (RCT), and normal prothrombin time (PT) and reptilase time (RT). Comparing the prolongation of APTT of samples containing the fluid to those containing a commercial heparin, the fluid contained an anticoagulant activity equivalent to 0.436 +/- 0.03 unit heparin per ml (mean +/- SEM, n = 14). In addition to prolonging the APTT, TT and RCT, the fluid also inhibited the clotting and amidolytic activities of thrombin. "Heparsorb" had nearly completely neutralized the anticoagulant activity in fluid samples, while protamine sulfate was only partially effective. Incubation of fluid with pronase or phospholipase did not affect its anticoagulant activity; incubation with heparinase had only a minimal effect. Electrophoresis of an alkali digested fluid on cellulose acetate revealed the presence of heparan sulfate. The native ascitic fluid also contained other hemostatic components including platelets, fibrinogen and antithrombin III, but their concentrations were much lower than in blood. Apparently, heparan sulfate in the neoplastic effusion is largely responsible for the bloody ascites tumor remaining unclotted.
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PMID:Anticoagulant activity in cell-free peritoneal fluid of an experimental pancreatic ascites tumor. 300 55

A new method to determine plasmaprokallikrein independently of its inhibitors is described. By ion exchange chromatography with DEAE-A-50 Sephadex plasmaprokallikrein can be separated from its inhibitors Cl-esterase inhibitor, alpha 2-macroglobulin, alpha 1-antitrypsin (protease inhibitor) and antithrombin III as well as from other enzymes like plasmin, Hagemann factor and glandular kallikrein, which can interfere with the chromogenic substrate of the amidolytic assay (S 2302) used to determine plasmakallikrein activity. Furthermore, this method also allows the measurement of plasmaprokallikrein in heparinized plasma, since heparin was separated by this chromatography technique from plasmaprokallikrein too. The enzymatic activity of activated plasmakallikrein was not changed by the ion exchange chromatography. Normal values of the plasmaprokallikrein content in plasma were in the range of 2.57 +/- 0.12 U/ml of plasma (n:42; X +/- SEM). No influence on plasmaprokallikrein activity of age and sex was found.
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PMID:Measurement of plasma prokallikrein independent of inhibitors and interfering enzymes. 364 44

Although the biological function of histidine-rich glycoprotein (HRG) is unknown, it may serve as an antifibrinolytic agent by interfering with the binding of plasminogen to fibrin. To define the role of HRG, plasma titers were measured by single radial immunodiffusion in eleven patients with thromboembolism before and after streptokinase (SK) therapy and were found unchanged (84.7 +/- 6.2%, M +/- SEM before, and 99.5 +/- 6.3% after 12 hr of SK therapy). The HRG peaks on crossed immunoelectrophoresis before and after SK infusion were also unchanged. Alpha 2-plasmin inhibitor fell during SK infusion as measured immunologically (102.0 +/- 15.0% before and 28.0 +/- 1.6% after 12 hr of therapy) and fibrinogen-fibrin degradative products appeared (mean titer of 1:2,048 after 12 hr of therapy), indicating that the infused SK was biologically active. Plasminogen levels before therapy were normal, as measured functionally and immunologically (105.4 +/- 4.9% and 96.0 +/- 5.6%, respectively), and both decreased after 12 hr of SK therapy (15.2 +/- 5.6% and 50.8 +/- 4.3%). No changes in functional antithrombin III titer, Hageman factor antigen level, or fibrinogen concentration, as measured turbidimetrically, were observed. Thus, although these data do not allow one to make any firm conclusions regarding the physiologic role of this protein in fibrinolysis, they do not exclude its increased catabolism, compensated by increased production, in patients undergoing fibrinolytic therapy.
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PMID:Histidine-rich glycoprotein and changes in the components of the fibrinolytic system after streptokinase therapy in patients with pulmonary thromboembolism. 401 25


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