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

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

Five subjects were injected with 5,000 IU of commercial heparin and low-molecular-weight heparin at an interval of 20 days after each injection. Both heparins produced the same platelet factor 4 release immediately after administration (commercial heparin 114.6 +/- 21.6 ng/ml, low-molecular-weight heparin 113.1 +/- 22.1 ng/ml). However, commercial heparin induced a more evident potentiating effect on ADP-induced platelet aggregation and was still present 60 min after injection. Low-molecular-weight heparin had a higher anti-Xa-specific activity than that determined by activated partial thromboplastin time. The opposite was true for the commercial preparation.
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PMID:Effects of low-molecular-weight heparin on platelets as compared with commercial heparin. 649 94

Bleeding time in rats was markedly prolonged after the administration of the water extract of Hsien-Ho-T'sao. This antihemostatic effect was more marked in the group of i.p. injection of the drug than in the group of p.o. administration for 2 or 7 consecutive days. Blood coagulation studies showed that plasma prothrombin time, activated partial thromboplastin time and stypven time were prolonged, while thrombin time and fibrinogen level were not changed. The thromboelastographic recording showed that reaction time was prolonged and maximal elasticity of clot was decreased. In addition, ADP- and collagen- induced aggregations of platelet-rich plasma were suppressed. In conclusion, the prolongation of the bleeding time might be due to both anticoagulant and antiplatelet action of the drug.
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PMID:Antihemostatic effect of Hsien-Ho-T'sao (Agrimonia pilosa). 649 95

T-2 toxin produced significant coagulation abnormalities when administered parenterally to Hartley strain guinea pigs. The animals developed depressed activity of all coagulation factors except fibrinogen. Platelet aggregation in whole blood was depressed in response to ADP and collagen. The animals also exhibited an initial rise followed by a fall in hematocrit level, leukocytosis, and a decrease in platelet count. These changes were detectable within hours of toxin administration, reached a maximum at 24 hr, and returned to normal over the next 2 days. Pretreatment of animals with vitamin K1 had no effect on the activity of coagulation factors. The activated partial thromboplastin time of dilutions of plasma from animals given T-2 toxin with plasma from control animals revealed a pattern which pointed to a deficiency of coagulation factors as the principal cause of prolonged clotting times in treated animals. The presence of a weak circulating anticoagulant could not be ruled out. The addition of T-2 to plasma and blood of normal animals in a concentration of 1 microgram/ml had no effect on clotting times or platelet aggregation.
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PMID:The hemostatic derangement produced by T-2 toxin in guinea pigs. 650 72

Factor Xa binds to platelets provided that factor Va is present on the platelet surface, an interaction that results in a striking acceleration of the conversion of prothrombin to thrombin. Thrombin then initiates fibrin formation, induces platelet aggregation, and stimulates the intraplatelet synthesis of thromboxane A2 (TXA2). Addition of thrombin (2.4-14.4 nM) to platelet-rich plasma increased the basal level of TXA2, measured as thromboxane B2, from less than 0.5 pmol per 10(8) platelets to (mean +/- SEM) 100 +/- 22 and 250 +/- 10 pmol per 10(8) platelets, respectively. Treatment of platelet-rich plasma with increasing concentrations of factor Xa (1-12 nM) prior to the addition of thrombin progressively inhibited the production of TXA2. Thrombin (9.6 nM), which produced 93% of the maximal formation of TXA2, was inhibited 70% by factor Xa (10 nM). To identify which of these steps in thromboxane synthesis was inhibited by factor Xa, platelets labeled with [14C]arachidonic acid were exposed to thrombin and products of prostaglandin synthesis were separated by thin-layer chromatography. In contrast to the inhibition of TXA2 synthesis, prostaglandin E2 and prostaglandin F2 alpha synthesis were not inhibited suggesting that neither phospholipase(s) nor cycloxygenase was involved. The inhibition of TXA2 formation by factor Xa could be reversed by increasing the molar ratio of thrombin to factor Xa to 5.5. Incubation of platelets with an IgG fraction of a human monoclonal antifactor V antibody, previously shown to inhibit factor Xa binding, was found to block factor Xa inhibition of TXA2 synthesis. The inhibition of TXA2 synthesis requires the presence of the active site serine of factor Xa and is not specific for TXA2 formation induced by thrombin because it is also demonstrable when the agonist is ADP. Further, factor Xa does not require additional plasma components for its action because its inhibitory effects are detected in gel-filtered platelets. The effect of factor Xa was evident at physiological (1.3 mM) calcium concentrations. These results indicate that factor Xa binding to platelets through factor Va not only stimulates thrombin formation but also has a countervailing effect by inhibiting TXA2 formation.
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PMID:Inhibition of thromboxane A2 synthesis in human platelets by coagulation factor Xa. 657 68

Treatment of blood coagulation factor Xa with insolubilized hexyl-agarose derivative of prostaglandin E1 (PGE1) results in the generation of two sulfhydryl groups in the protein molecule. The reduced factor Xa was found to be a potent inhibitor of platelet aggregation and thromboxane A2 synthesis induced by ADP. In contrast to the inhibition of thromboxane formation, the reduced factor Xa had no effect on the formation of PGE2 indicating that thromboxane synthetase might be selectively inhibited by the reduced factor Xa. Incubation with oxidized glutathione reversed the inhibitory activity of factor Xa previously exposed to the insolubilized hormone. Soluble PGE1 also reduces factor Xa, but more slowly than the insolubilized PGE1. PGE1 also exhibits reducing ability as tested with redox dyes. Reduction of factor Xa by dithiothreitol also transformed the coagulation factor into an inhibitor of platelet aggregation and thromboxane A2 formation. These experiments indicate that reduction of factor Xa leads to a reversible alteration of the molecule which inhibits platelet aggregation induced by ADP. This effect of reduced factor Xa is probably mediated through the inhibition of thromboxane A2 synthesis.
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PMID:Inhibition of ADP-induced platelet aggregation by reduced factor Xa. 661 61

The effect of ketoprofen (Orudis, Farmitalia) on ADP, epinephrine (EPI) and collagen (COLL) induced platelet aggregation (PlA), simplate bleeding time (SBT), partial thromboplastin time (PTT) and per cent prothrombin activity (PrA) was studied in eleven patients, four males and seven females (median age 59 years) with rheumatoid arthritis (six cases), cancer (four cases) and osteoarthrosis (one case). Tests were performed before and 1, 8 and 24 hours after a single intravenous dose (600 mg) of ketoprofen and on Days 4 and 8 during a 7-day treatment (200 mg i.v. every 8 hours) and 1 day after withdrawal of the drug. PTT and PrA were not affected by the drug. Bleeding time was not significantly modified by the acute treatment, but was prolonged during the subacute course, though it was not different from baseline values at the end of the trial. Significant reduction of platelet aggregation was seen in both acute and subacute conditions with complete or almost complete recovery 36 hours after the last dose. It is concluded that ketoprofen affects platelets with readily reversible inhibition of in vitro aggregation and a slight increase of bleeding time.
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PMID:Effects of intravenous high doses of ketoprofen on blood clotting, bleeding time and platelet aggregation in man. 661 83

In 12 chronically anticoagulated patients the administration of 1-p-chlorobenzoyl-5-methoxy-2-methyl-3-indoacetohydroxamic acid (oxametacin, Flogar), three times 100 mg a day, decreased the thrombotest percentage from a mean of 11.2% to a mean of 8.3% after one week and of 7.8% after two weeks of treatment. A potentiating effect of oxametacin was also found when the prothrombin time or the activated partial thromboplastin time were used as parameters. In one third of our patients an adaptation of the coumarin dose or even an interruption in the warfarin administration was necessary. Although no severe bleedings occurred, care should be taken in prescribing oxametacin to anticoagulated patients. In a second part of this study we compared the ex vivo effects of a single oral dose of 1 g of acetylsalicylic acid, 50 mg of indometacin and 100 mg of oxametacin in human volunteers. Platelet aggregation and 5HT--14C release induced by collagen. Thrombofax, ADP, adrenaline (epinephrine), bovine plasma and ristocetin were measured before, 1 and 24 h after drug administration. A clear-cut inhibitory effect as induced by acetylsalicylic acid was not found for oxametacin.
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PMID:Effects of oxametacin on coumarin anticoagulation and on platelet function in humans. 668 67

Differences in blood coagulating and fibrinolytic abilities before and after delivery were investigated in order to elucidate the changes occurring at the delivery time in increased blood coagulation and inhibited fibrinolytic condition during pregnancy, especially in its latter period, and the relation between the amount of intrapartum hemorrhage and blood coagulating and fibrinolysis before delivery was examined in order to predict hemorrhage. Twenty-one women who had no complications in pregnancy or delivery and gave birth by vaginal spontaneous delivery with not more than 500ml of intrapartum hemorrhage (normal hemorrhage group) and 7 women who gave birth by vaginal spontaneous delivery with not less than 501ml of abnormal intrapartum hemorrhage (abnormal hemorrhage group) were used as the objects of study, and coagulating and fibrinolytic abilities were examined. The result obtained are summarized as follows: Differences in blood coagulating and fibrinolytic abilities before and after delivery tended to be similar in both normal and abnormal hemorrhage groups. Platelet count and fibrinogen content were decreased, activated partial thromboplastin time became shorter, compared with those examined before delivery, and these appeared to be an increase in blood coagulating ability after delivery. Fibrinolytic ability was seen to be not remarkably different before and after delivery. Fibrinolytic ability was seen to be not remarkably different before and after delivery. Platelet ADP and epinephrine aggregation were reduced after delivery, but platelet collagen aggregation showed no change. As for blood coagulating and fibrinolytic abilities before delivery, prothrombin time was shorter in the abnormal hemorrhage group than in the normal hemorrhage group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Blood coagulation and fibrinolysis in spontaneous delivery]. 671 32

Extracts of adult Ancylostoma ceylanicum prolonged the prothrombin time (PT) and partial thromboplastin time with kaolin ( PPTK ) of both human and dog plasmas in vitro. Excretory/secretory (E/S) products of these worms had similar effects while larval extract prolonged the PTTK only. Thus, the anticoagulant activities of this parasite are dependent upon the stage of the worm's life cycle. Collagen- and ADP-induced platelet aggregation were inhibited by adult and larval extracts. When the peripheral blood and bleeding times of dogs with varying worm burdens were examined, the only abnormality was shortening of the PTTK in the most heavily infected animals. Homogenates of dog small bowel subjacent to adult hookworms prolonged the PT of dog plasma and electron microscopical examination of this tissue revealed aggregation of platelets in blood venules without fibrin deposition. Thus, this study provides evidence that the anticoagulant properties of hookworms may have biological significance in infected animals.
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PMID:The anticoagulant effects of the hookworm, ancylostoma ceylanicum: observations on human and dog blood in vitro and infected dogs in vivo. 674 May 54

Platelet-poor plasmas (PPPs) from 52 out of 71 patients affected by different diseases and selected for increased amounts of circulating platelet aggregates, incubated at 37 degrees C for 30 min with control platelet-rich plasma (PRP; cross-matching test) induced the formation of platelet aggregates, stimulated the production of malondialdehyde and enhanced ADP-induced aggregation. 31 control PPPs were consistently negative at cross-matching test. Gel chromatography of plasmas on agarose 4% allowed the identification of four different fractions (A, B, C, D) provided with aggregating activity. Fraction A eluted at the void volume was to be identified with the von Willebrand factor, whereas B, C and D fractions, eluted at the same elution volumes as activated factor X were mainly composed of factor X (fraction B) and activated factor X (fractions C and D). Thrombin activity was absent in all the fractions provided with aggregating activity. Also, from control PPPs negative at cross-matching tests, the same fractions could be obtained, although of 5--10 times lower aggregating potency, thus explaining the negative cross-matching tests. These findings stress the role of some extraplatelet factors related to hypercoagulability in platelet hyperaggregability.
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PMID:Increased platelet aggregation due to plasma-aggregating activity. Identification of the responsible factors. 676 58


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