Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.21.6 (thromboplastin)
 13,278 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Gastric lesions occurred spontaneously and were increased in number by seven hours of restraint stress in rats with portal vein constriction (PVC). Vagotomy and pyloroplasty protected the congested stomach from erosion formation with stress. Major weight loss occurred two days after PVC, but not thereafter. Platelet counts were decreased in intact and splenectomized rats with portal hypertension, but prothrombin time, partial thromboplastin time, and fibrinogen were unaffected, and histological stains failed to demonstrate thrombin in the gastric blood vessels. The oxygen pressure (PO2) of the gastric luminal fluid was decreased at day 2, but was normal at day 4 after PVC. Hypersection of acid and abnormal acid equilibration were not observed in the stomach. Gastric congestion, weight loss, and possibly portasystemic shunting of blood contributed to the higher incidence of gastric erosions with portal hypertension.
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PMID:Portal hypertension and gastric lesions in the rat. 0 51

The macromolecular breakdown products of fibrinogen are known mainly for their inhibitory effect on the clotting of fibrinogen by thrombin. This inhibitory effect is due to interference with both the proteolytic action of thrombin and the polymerization of the fibrin monomers. However, the action of these products is not limited to these effects. They can on the one hand inhibit the consumption of Factors II and XIII and promote the inactivation of Factor VIII by thrombin. On the other hand, they can potentiate the activation of prothrombin in purified systems via the intrinsic pathway. The incidental observation was also made that Factor IXa and or Factor Xa inactivate Factor VIII. As substrates of both thrombin and plasmin the large fragments protect these two enzymes from spontaneous inactivation, while at the same time they inhibit their respective proteolytic activities. Contradictory results were obtained regarding their effect on platelets. The micromolecular (dialyzable) breakdown products prolong the thrombin, prothrombin, and partial thromboplastin times of plasma and retard the generation of the intrinsic prothrombin activator. They can also potentiate the effects of biologically active peptides and amines on the smooth muscles and on vascular permeability.
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PMID:Physiological effects of the plasminolytic derivatives of fibrinogen. 0 46

The in vitro effects of N-3-(1-benzyl-cycloheptyloxy)-propyl-N,N-dimethylammonium-hydrogenfumarate (bencyclan) on clotting, fibrinolytic and platelet function test were investigated by adding the drug to normal human plasma. An anticoagulant activity, mainly of an antithromboplastin nature (directed against later stages of intrinsic thromboplastin formation and against tissue thromboplastin), was observed, while thrombin phase was unaffected. No effect was found in the fibrinolytic system tested (euglobulin lysis, UK-activated fibrinolysis, "hanging clot" method). The drug, although capable of aggregating platelets by itself at very high concentrations, showed a striking inhibitory effect, over a wide range of concentrations, both on platelet aggregation induced by ADP, epinephrine or collagen and on platelet adhesiveness to glass or collagen. Clot retraction was also clearly inhibited. PF3 availability was influenced with a peculiar two-phase behaviour dose-dependently. High concentrations showed a promoting action, while the lower were obviously inhibitory. It is suggested that the effects on platelet function may be due to an influence of the drug on cell membrane.
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PMID:In vitro effects of bencyclan on coagulation, fibrinolysis and platelet function. 1 70

In the rabbit the application of a non-lethal, sleep-inducing dose of bromisovalerianyl carbamide (0.5 g/kg body weight) causes an activation of the coagulation system. This activation is manifested by shortened thrombin and partial thromboplastin times and a decrease of fibrinogen concentration and Factor V activity. In contrast, pentobarbital sodium at a dose (62.5 mg/kg) which causes the same changes in arterial partial oxygen pressure and arterial pH does not influence the coagulation system. The bromocarbamide-induced changes in the coagulation system are not to be considered as a result of hypoxia and acidosis but seem to be caused by early endothelial and tissue lesions which result in the release of procoagulatory substances. In healthy test persons a single dose of 1.5 g bromisovalerianyl carbamide has no demonstrable influence on the system of hemostasis.
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PMID:The activation of intravascular coagulation by bromocarbamide. 1 52

Human alpha-thrombin, the thromboplastin activation product of prothrombin with high clotting and esterase activity, was produced from Cohn Fraction III paste. The procedure started with 0.4 to 3.2 kg of frozen paste and was completed in 2 or 3 days. Some 23 g of thrombin were recorded for 65 quantitated preparations made from 11 lots of Fraction III paste. These preparations were obtained at protein concentrations of 3.9 +/- 1.3 mg/ml with a yield of 340 +/- 110 mg/kg of paste, which represented 48 +/- 14% of the clotting potential extracted as prothrombin. They had specific clotting activities of 2.8 +/- 0.4 U.S. (NIH) units/microng of protein and titrated to 88 +/- 8% active with p-nitrophenyl-p'-guanidinobenzoate (NPGB). Those (N - 29) examined by labeling with [14C]diisopropyl phosphorofluoridate (iPr2P-F) and electrophoresing in sodium dodecyl sulfate (SDS)-polyacrylamide gels were found to contain only (N = 4) or predominantly alpha-thrombin (97 +/- 3%) and corresponding amounts of ists degradation product, beta-thrombin (2.6 +/- 3.1%). No plasmin(ogen), prothrombin complex factors (II, VII, IX, IXalpha, X, Xalpha), or prothrombin fragments were detected in representative preparations. As produced in 0.75 M NaCl, pH approximately 6, thrombin was stable for approximately 1 week at 4 degrees and for greater than 1 year at less than or equal to 50 degrees; freeze-dried thrombin stored at 4 degrees for greater than 1 year displayed stable clotting activity and no vial to vial variation, permitting its use for reference purposes. Human thrombin generated by Taipan snake venom activation was compared with that produced by rapid thromboplastin activation: after treatment with [14C]iPr2P-F, greater than 95% of the label in both thrombins migrated at the same rate during electrophoresis in SDS; identical pairs of NH2-terminal residues were released in three consecutive Edman degradation cycles.
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PMID:Human thrombins. Production, evaluation, and properties of alpha-thrombin. 1 8

The potential differences in hematologic profiles of blood samples drawn simultaneously from the right utero-ovarian vein and from the upper extremity were investigated in four patients with uncomplicated molar pregnancy in stable obstetric conditions. The patients had undergone no previous chemotherapy and were scheduled for total abdominal hysterectomies. The dominant abnormalities in uterine venous blood were prolongation of thrombin time; shortening of activated partial thromboplastin time; positive protamine sulfate test; and increase in coagulation factors II and VII, with a tendency to low values in factor V. Peripheral samples gave almost parallel results in all altered and normal tests, except in one case with very striking differences in factors II, V, VII and X. Several local and systemic influences are discussed. It is concluded that molar pregnancy seems to have important systemic mechanisms affecting the stability of the blood coagulation homeostasis, which act in addition to those at a local level.
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PMID:Uterine and peripheral hematologic profiles in molar pregnancy. 3 41

By devising and applying quantitative methods for the assay of thrombin and autoprothrombin C and by developing techniques for their purification, it was possible to obtain information about the function and properties of antithrombin. The inhibitor is a protein for which the initial purification steps consist of removing fibrinogen from plasma by heating to 56 degrees for 3 min, removing prothrombin complex by absorption on barium carbonate, absorbing the antithrombin on aluminum hydroxide, and eluting with phosphate buffer. Antithrombin is limited in its capacity to neutralize thrombin activity, and, under some conditions, the rate of inhibition was accelerated, but equivocal results were involved. Heparin cofactor was found to be essential for retarding the formation of thrombin, and, by inference, it is essential for retarding the formation of autoprothrombin C. Heparin cofactor and antithrombin III are the same. Thrombin absorbs on fibrin, and this has been referred to as the "antithrombin I effect." Interference with the thrombin-fibrinogen reaction by mixtures of antithrombin III and heparin is called the "antithrombin II henomenon." The acceleration of thrombin inactivation at the time thrombin forms is called the "antithrombin IV effect." It was discovered that antithrombin III neutralizes thrombin, as well as autoprothrombin C. The inhibitor and the enzyme form a mutual depletion system. To assay for antithrombin III, a standard quantity of thrombin (about 1,100U/ml) was reacted with antithrombin III for 2 hr. The percent thrombin inactivated was then measured. In random samples of human blood, a wide range of antithrombin III concentration was found. The inhibitor is relatively stable in plasma and serum. It is not changed in concentration when Dicumarol therapy is instituted. Ether extraction of plasma reduces antithrombin III activity. Seitz filtration of plasma did not remove activity. Under special conditions, antithrombin III enhances esterase activity of thrombin. Under special conditions, thrombin regenerates from the thrombin-antithrombin III complex. Antithrombin III neutralizes the activity of prethrombin-E and thrombin-E; consequently, an active histidine center found in the B1 chain of thrombin is not essential for the binding of antithrombin. Autoprothrombin II-A activity was neutralized by antithrombin III. Autoprothrombin C was found to be neutralized by antithrombin III; the amounts required varied with the molecular forms of autoprothrombin C. Thrombin and autoprothrombin C apparently occupy the same binding sites on antithrombin III. An equation was developed to account for all the known characteristics of antithrombin III functions. The kinetic aspects of thrombin neutralization were found to correspond exactly with those of autoprothrombin C. Antithrombin III is a high-capacity inhibitor of the two most powerful enzymes in blood coagulation.
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PMID:Antithrombin III: a backward glance o'er travel'd roads. 4 4

Antithrombin III, purified to homogeneity according to polyacrylamide gel disc electrophoresis and immunoelectrophoresis, inhibited the activity of purified factor IXa and Xa, whereas factor VII was not inhibited either in the active or in the native form. Antithrombin III is the single most important inhibitor of factor Xa in plasma. Factor Xa does not, however, reduce the activity of antithrombin III against thrombin.
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PMID:The effect of antithrombin III on the activity of the coagulation factors VII, IX and X. 6 31

The determination of the onset of a disseminated intravascular coagulation (DIC) is examined shortly after its intraoperative andpost-operative dissolution with the help of easily performable haematological and physiological clotting tests in 20 patients. In this connection the operation is appreciated as a model even for other processes defined at the beginning, where DIC can be observed. Whereas the aethanol test, the determination of fibrinogen split products (FSP) and the euglobulin lysis time indicate the beginning of DIC more clearly in the form of average values, the aethanol test, partial thromboplastin time and thrombin time have a prognostic value for each patient. As it is too time consuming to determine FSP, the counting of basophilie granulocytes may be used for the diagnosis. In the initial phase of and post-operative DIC will determine the essential share of predisposition to post-operative thromboembolism.
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PMID:[On the causes of intra- and post-operative consumption coagulopathies and postoperative thromboembolism]. 7 15

The influence of hemofiltration on the number of platelets and on coagulation factors was investigated in patients with chronic renal insufficiency. These investigations were done on 12 patients during 22 treatments with hemofiltration. Blood samples were taken before hemofiltration, 10, 30 and 120 minutes after the beginning of the treatment and at the end of hemofiltration. In comparison to the original values we found a loss of platelets, a small decrease in the concentration of fibrinogen and a small increase in the fibrin monomer complex, plasminogen, antithrombin III, alpha1-antitrypsin and in alpha2-macroglobulin. The thrombin time, the partial thromboplastin time and Quick's test showed that the blood of these patients contained sufficient hepatin. Use of fibrin plates (Astrup) showed no signs of fibrinolytic activity. Compared to the results, which were obtained some years ago during hemodialysis, we found a smaller extent of alterations of blood coagulation factors and number of platelets.
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PMID:Alterations of clotting factors and platelets during hemofiltration. 7 95


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