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)

Infections due to Streptococcus pneumoniae and products from the organism have been associated with alterations in blood clotting and function of platelets. Pneumococci and pneumococcal polysaccharide shortened the clotting times of whole blood, platelet-rich plasma (PRP), and platelet-poor plasma (PPP) in vitro. Clotting times of PPP and PRP from C6-deficient animals were likewise decreased. The bacteria had no effect on the one-stage prothrombin time or the partial thromboplastin time when the organisms were used as activating agents. Platelets aggregated in the presence of pneumococci, but aggregation was prevented by the addition of cyclic adenosine 3', 5'-monophosphate (cAMP). Furthermore, cAMP corrected the shortened clotting time of PRP in the presence of pneumococci. The clumping and release of polymorphonuclear coagulant that was induced by pneumococci was not prevented by cAMP. Thus, pneumococci exert several dose-dependent thromboplastic effects: (i) release of platelet thromboplastic substances; (ii) a direct thromboplastic effect; and (iii) release of polymorphonuclear coagulant.
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PMID:Effect of pneumococci on blood clotting, platelets, and polymorphonuclear leukocytes. 0 Mar 31

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

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

After observing that lavage of the stomach with alkaline solutions has a beneficial effect on the control of gastric hemorrhage, we examined the platelet and coagulation factor activities under conditions of lower and elevated pH. The results showed that change of the pH from acidosis to 7.0 and even to slight alkalosis induces platelet aggregation, platelet calcium and serotonin release, as well as platelet factor II availability. The prothrombin and partial thromboplastin times approached normal levels, whereas the fibrinogen level did not change significantly. The results obtained may serve as an explanation for the control of the intragastric bleeding in patients treated by maintenance of their gastric pH at 7.0.
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PMID:The effect of pH on platelet and coagulation factor activities. 2 78

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

Synthetic cyclic growth-hormone release-inhibiting hormone (G.H.-R.I.H.) impaired platelet aggregation in each of four healthy men given 6-hour infusions. The effects lasted over 24 hours in three of them. There was no consistent change in platelet-counts during the infusions, but 18 hours after the end of the infusions there was a slight but significant increase in platelet-count. There was no change in prothrombin-time, partial thromboplastin-time, fibrinogen titres, and fibrinogen-degradation products. Incubation of G.H.-R.I.H. with blood in vitro did not affect platelet aggregation. Similar impairment of platelet function has been reported by others in baboons given linear G.H.-R.I.H. Infusions in the four healthy men studied also produced abdominal pain, dizziness, and diarrhoea in three, as have been reported in patients similarly infused. Although other side-effects or impairment of platelet-counts or bleeding-tendencies have not been reported in patients infused for up to 72 hours, caution should be exercised when using G.H.-R.I.H. over extended periods until further data on its toxicity are available.
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PMID:Impairment of platelet function by growth-hormone release-inhibiting hormone. 4 78

Intravenous administration of BSA into 3-month-old rabbits producing detectable anti-BSA antibody only of the IgE class of immunoglobulin induced a variety of intravascular blood coagulation alterations observed in the plasma 15 min after antigen challenge included: a) the intravascular consumption of intrinsic blood coagulation factors XII, XI, and IX and possibly the reduction in clottable fibrinogen; b) a significant prolongation of the activated partial thromboplastin time but not the prothrombin time; and c) the production of an inhibitor affecting the last stage of blood coagulation. The observed blood coagulation alterations were not caused by the manipulative procedures utilized, the presence of anti-BSA, IgG or IgM antibody, histamine-induced alterations in the vascular endothelium or the development of hypotensive shock. It is proposed that specific IgE antibody can induce directly or indirectly the activation of intrinsic blood coagulation in vivo.
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PMID:IgE-induced blood coagulation alterations in the rabbit: consumption of coagulation factors XII, XI, and IX in vivo. 5 Mar 67

A total of 23 leukaphereses were performed on five normal, healthy donors for the purpose of providing granulocyte transfusions to septic leukemia patients with granulocytopenia. Dexamethasone 7.25 to 7.50 mg was given orally 10 to 12 hours prior to each donation, and an average of 304 ml of hydroxyethyl starch (HES) was given intravenously during each procedure. During the period of observation for each donor, there was no significant change of total leukocyte and platelet counts, total bilirubin, alkaline phosphatse, LDH, SGOT, creatinine, BUN, and uric acid determinations. Changes in the concentrations of serum protein, albumin, cholesterol, and glucose were thought to be due to hemodilution. Partial thromboplastin and prothrombin times remained within normal limits following collection procedures. Hemoglobin levels decreased transiently following the first three leukaphereses in all donors, but fell progressively to 11.8 gm/dl in one donor undergoing seven procedures in a 35-day period. Dexamethasone and HES in these doses can be given safely to multiply leukapheresed donors.
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PMID:The safety of dexamethasone and hydroxyethyl starch in the multiply leukapheresed donor. 5 93

The effect on abnormal coagulation tests of infusions of fresh-frozen plasma (F.F.P), prothrombin complex concentrates, and a combination of these treatments was compared in 30 patients with chronic liver disease undergoing needle biopsy. A single dose of F.F.P. (12 ml/kg body-weight) was found to be the least effective therapeutic regimen. The concentrate containing factors II, IX, and X was also not adequate, but the additional administration of factor-VII concentrate corrected the prothrombin-time (P.T.) and "Normotest" (N.T.) in most patients. However, this regimen did not correct the prolonged kaolin activated partial thromboplastin-time (K.P.T.T.). The results of tests for exploring both the extrinsic (P.T. and N.T.) and intrinsic (K.P.T.T.) coagulation systems only became normal after the combined administration of a lower dose of F.F.P. (8 ml/kg body-weight) and of both concentrates (12 units/ml). There was no clinical or laboratory evidence of thrombotic complications. No patient developed acute hepatitis or hepatitis-B surface antigen in the twelve months after biopsy. These results indicate that prothrombin-complex concentrates in combination with F.F.P. may therefore be used to allow liver biopsy to be performed safely in patients presenting with severe coagulation defects.
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PMID:Correction of abnormal coagulation in chronic liver disease by combined use of fresh-frozen plasma and prothrombin complex concentrates. 6 Jun 23


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