The Effects of Leguminous Seed Extracts on Blood Coagulation

1962 ◽  
Vol 08 (02) ◽  
pp. 256-269
Author(s):  
R. J Speer ◽  
J. L Porter
Keyword(s):  
Factor Viii ◽  
Prothrombin Time ◽  
Blood Coagulation ◽  
Factor Ix ◽  
Factor Vii ◽  
Clot Lysis ◽  
Factor V ◽  
Leguminous Seed ◽  
Recalcification Time ◽  
Clot Time

SummaryThe saline extracts of one hundred leguminous seed were screened for their effect on blood coagulation by the following tests: thrombin clot time, recalcification time, Quick prothrombin time, clot lysis and clot retraction. Nineteen of these extracts, when reacted with normal plasma, gave a prolonged clot time in at least one of two tests: recalcification time and Quick prothrombin time. The eight which gave a prolonged Quick prothrombin time were tested for inhibition in the following assay systems: Factor V, factor VII-complex, and prothrombin. All nineteen, including the seventeen which prolonged the re-calcification time and the two which did not, were tested for their inhibitory action in the following assay systems: Factor VIII, factor IX, and plasma thromboplastin antecedent.The inhibition of prothrombin, factor V, and factor VII-complex was mild and not specific for any of these factors. Factor V activity was depressed more than the other two. By contrast, the inhibition of factor VIII, factor IX, and plasma thromboplastin antecedent was very strong and demonstrated a relatively high degree of specificity.

Occult intravascular clotting by means of intravenous injection of thrombin

1959 ◽  
Vol 197 (4) ◽  
pp. 791-794 ◽  
Author(s):  
Armand J. Quick ◽  
Clara V. Hussey ◽  
John Harris ◽  
Kenneth Peters
Keyword(s):  
Factor Viii ◽  
Prothrombin Time ◽  
Intravenous Injection ◽  
Factor Ix ◽  
Capillary Network ◽  
Factor Vii ◽  
Factor V ◽  
Dilute Solution ◽  
Progressive Decrease ◽  
Stable Factor

On infusing a dilute solution of thrombin intravenously into a dog at a constant and carefully regulated rate, no massive thrombosis occurs and no evidence of a thrombo-embolic state is obtained. An occult type of intravascular clotting is produced which is characterized by a progressive decrease of the level of fibrinogen, thrombocytopenia, a prolonged prothrombin time and a poor consumption of prothrombin. Labile factor (factor V) and thromboplastinogen (factor VIII) are strikingly diminished. Prothrombin is moderately decreased while stable factor (factor VII) and PTC (factor IX) are not significantly affected. It is postulated that the adsorption of thrombin to the fibrin fibrils which are filtered off in the capillary network and destroyed, constitutes the principal means for preventing dangerous accumulation of thrombin in the blood.

Coagulation Findings in Rats with Experimental Hypersplenism and Their Changes after Splenectomy and after Administration of Adrenaline

1970 ◽  
Vol 23 (03) ◽  
pp. 593-600
Author(s):  
P Pudlák ◽  
I Farská ◽  
V Brabec ◽  
V Pospíšilová
Keyword(s):  
Factor Viii ◽  
Normal Control ◽  
Normal Values ◽  
Coagulation Factors ◽  
Factor Vii ◽  
Factor V ◽  
Thrombin Time ◽  
Factor Ii ◽  
Recalcification Time

Summary1. The following coagulation changes were found in rats with experimental hypersplenism: a mild prolongation of the recalcification time, shortened times in Quick’s test, a lowered activity in plasma thrombin time and shortened times in the partial thromboplastin test. Concentrations of factor II, V, VII (+X), VIII and X did not differ from those of normal control rats.2. The administration of adrenaline to hypersplenic rats induced the correction of the partial thromboplastin test, Quick’s test and plasma thrombin time to normal values. Concentrations of coagulation factors were not significantly changed. An increase was found in factor V.3. Splenectomy performed in hypersplenic rats was followed by a shortened recalcification time, a prolongation of the partial thromboplastin test and of the test with partial thromboplastin and kaolin. A prolongation was also observed in Quick’s test. Complete correction of plasma thrombin time was not observed. The concentration of factor VII increased.4. The administration of adrenaline to splenectomized rats with experimental hypersplenism did not induce any significant changes with the exception of a corrected plasma thrombin time and a decreased concentration of factor VIII.5. A different reaction of factor VIII to adrenaline in normal and hypersplenic rats is pointed out.

Multidimensional Similarity of Letters

1969 ◽  
Vol 28 (1) ◽  
pp. 3-12 ◽  
Author(s):  
Teodor Kuennapas ◽  
Anne-Jeanette Janson
Keyword(s):  
Factor Viii ◽  
Factor Ix ◽  
Factor Vii ◽  
Similarity Analysis ◽  
Factor V ◽  
Factor I ◽  
Considerable Portion ◽  
Lower Case ◽  
Factor Ii

28 lower-case letters of the Swedish alphabet were studied by the method of multidimensional similarity analysis. 57 Ss participated in the experiment. 9 factors were found. Factor I is called ‘t’ or ‘Vertical linearity,’ Factor II: ‘o’ or ‘Roundness,’ Factor III: ‘n’ or ‘Parallel vertical linearity,’ Factor IV: ‘i’ or “Vertical linearity with dot,’ Factor V: ‘p’ or ‘Roundness attached to vertical linearity,’ Factor VI: ‘k’ or ‘Vertical linearity with crossness,’ Factor VII: ‘a’ or ‘Roundness attached to a hook,’ Factor VIII: V or ‘Angularity open upward’ and Factor IX: ‘z’ or ‘Zigzaggedness.’ ‘Vertical linearity’ and ‘Roundness’ are the most important of these factors and account for a considerable portion of the similarity among many letters.

Studies on the Fate of Coagulation Factors during the Clotting of Normal and Pathological Blood

1959 ◽  
Vol 03 (04) ◽  
pp. 578-587
Author(s):  
Cecil Hougie
Keyword(s):  
Blood Coagulation ◽  
Hemophilia A ◽  
Coagulation Factors ◽  
Factor Ix ◽  
Hemophilia B ◽  
Factor Vii ◽  
Normal Blood ◽  
Modern Concept ◽  
Factor V ◽  
Mild Case

SummaryIn a mild case of Stuart factor (SF) deficiency and in a patient with hemophilia B (factor IX deficiency) consumption of AHF (factor VIII) was normal but was abnormal in more severe examples of these diseases. This finding reconciles previously conflicting reports. Factor V utilisation was abnormal in moderately severe cases of SF deficiency, hemophilia A and hemophilia B but normal in mild cases of SF deficiency and hemophilia B. A mild case of hemophilia A was not studied. These findings would be expected from the modern concept of blood coagulation. However, the findings with respect to AHF are equally well explained if AHF is destroyed by some intermediate product of blood coagulation, such as thrombin, appearing at the time of the appearance of fibrin.The concentration of SF was found to remain constant during the clotting of both normal blood and blood deficient in factor VILThe concentration of factor VII during the coagulation of normal blood remained constant until the appearance of fibrin. The concentration then increased, but this finding was not consistently obtained. No abnormality in the fate of factor VII during the clotting of blood deficient in SF was found.

Molecular evolution of the vertebrate blood coagulation network

2003 ◽  
Vol 89 (03) ◽  
pp. 420-428 ◽  
Author(s):  
Colin Davidson ◽  
Robert Hirt ◽  
Kalpana Lal ◽  
Philip Snell ◽  
Greg Elgar ◽  
...  
Keyword(s):  
Blood Coagulation ◽  
Serine Proteases ◽  
Large Scale ◽  
Factor Ix ◽  
Supplementary Information ◽  
Factor Vii ◽  
Factor V ◽  
Factor X ◽  
Sequence Alignments ◽  
Comparative Sequence

SummaryIn mammalian blood coagulation 5 proteases, factor VII (FVII), factor IX (FIX), factor X (FX), protein C (PC) and prothrombin act with two cofactors factor V and factor VIII to control the generation of fibrin. Biochemical evidence and molecular cloning data have previously indicated that blood coagulation involving tissue factor, prothrombin and fibrinogen is present in all vertebrates. Using degenerate RT-PCR we have isolated and characterized novel cDNAs with sequence identity to the blood coagulation serine proteases and cofactors from chicken and the puffer fish (Fugu rubripes). Sequence alignments, phylogenetic and comparative sequence analysis all support the existence of the Gla-EGF1-EGF2-SP domain serine proteases FVII, FIX, FX, PC and the A1-A2-B-A3-C1-C2 domain protein cofactors FV and FVIII in these species. These results strongly suggest that the blood coagulation network is present in all jawed vertebrates and evolved before the divergence of tetrapods and teleosts over 430 million years ago; and that vertebrate blood coagulation may have benefited from two rounds of gene or whole genome duplication. Sequences identified in Fugu coding for additional FVII-like, FIX-like and PC-like sequences support the possibility of further tandem and large-scale duplications in teleosts. Comparative sequence analyses of amino acid residues in the active site region suggest these additional sequences have evolved new and as yet unknown functions.Supplementary information to this article available at both http://europium.csc.mrc.ac.uk and www.thrombosis-online.com

Generation Of Coagulation Factors By The Isolated Rat Liver Perfused With A Synthetic Blood Substitute

1981 ◽  
Author(s):  
C A Owen ◽  
E J W Bowie
Keyword(s):  
Factor Viii ◽  
Rat Liver ◽  
Blood Substitute ◽  
Factor Ix ◽  
Factor Vii ◽  
Clotting Factor ◽  
Isolated Perfused Rat Liver ◽  
Factor Xii ◽  
Factor V ◽  
Factor X

Measuring the release of small amounts of a clotting factor from an isolated perfused rat liver is difficult if the perfusate already contains some of the factor. Further, platelet-containing perfusates generate a coagulant activity that may invalidate clotting assays.We have successfully employed a completely synthetic blood substitute for rat liver perfusions. The perfusate is “Fluosol-43” generously furnished by Alpha Therapeutic Corporation. The oxygen-carrying perfluorochemical is FC-43 (perfluorotributylamine) and the substitute for albumin is hydroxyethyl starch. Using the Brauer perfusion technique, we found that rat livers in 5 hours released an average of 2.3% of the normal plasma concentration of prothrombin, 8.4% factor V, 16.2% factor VII, 7.0% factor IX, 3.7% factor X, 28.3% factor XI and 12.3% factor XII. Antithrombin III and plasminogen were also generated.Only minute amounts of factor VIII were released unless serum, cryoprecipitate or cryoprecipitate-free plasma was added; then the yield was 8.8% on average. The more “venom factor” (platelet aggregability with Bothrops alternata venom) added to the synthetic perfusate, the more factor VIII was released.

scholarly journals Experimental Hemostasis in Normal Dogs and Dogs with Congenital Disorders of Blood Coagulation

Blood ◽  
1967 ◽  
Vol 30 (5) ◽  
pp. 636-668 ◽  
Author(s):  
T. HOVIG ◽  
H. C. ROWSELL ◽  
W. J. DODDS ◽  
L. JØRGENSEN ◽  
J. F. MUSTARD
Keyword(s):  
Factor Viii ◽  
Blood Coagulation ◽  
Bleeding Time ◽  
Light And Electron Microscopy ◽  
Factor Ix ◽  
Surrounding Tissue ◽  
Factor Vii ◽  
Congenital Defects

Abstract Hemostasis was examined after transection of vessels, 50-200 microns in diameter, both in normal dogs and in dogs with congenital defects of either factor VII, factor IX, or factor VIII. The formation of the hemostatic platelet plugs was observed by direct microscopy in vivo, and sections of the plugs were prepared for both light and electron microscopy 10 to 30 minutes after transection. Furthermore, the reaction of platelets from normal and abnormal dogs with adenosine diphosphate, collagen and thrombin was tested in vitro by a turbidimetric technic. In normal and factor VII deficient dogs the initial arrest of bleeding took place about 3 minutes after transection, and rebleeding was infrequently observed. Their platelet plugs were composed of densely packed platelets, anchored to the vascular and perivascular tissue and surrounded by a cap of fibrin. In factor IX deficient dogs there was no definite prolongation of the initial bleeding time, but rebleedings were frequent. In factor VIII deficient dogs the initial bleeding time was prolonged and the intensity of the bleeding had a wave-like characteristic. The plugs in the hemophilic dogs were larger than normal, were rich in channels, and had areas of loosely packed platelets and an incomplete fibrin cap. Treatment of factor IX deficient dogs with Dicumarol did not further impair hemostatic plug formation in the doses used. Treatment of factor VII deficient dogs with heparin, or factor IX deficient dogs with phenylbutazone, prolonged the bleeding time markedly, delayed the building up of the plug, and gave fragile, loosely packed plugs. Treatment of normal dogs with phenylbutazone did not alter the hemostatic process at the dosage used. In the in vitro studies, platelets from the dogs with congenital coagulation defects reacted normally with the aggregating stimuli. It is concluded that the initial platelet interaction wih the vessel wall and surrounding tissue is not dependent upon blood coagulation. An intact intrinsic pathway of coagulation is necessary for the stabilization of the hemostatic plug after it is formed.

The Coagulation Defect in Hypervitaminosis A in Rats

1962 ◽  
Vol 07 (01) ◽  
pp. 159-168 ◽  
Author(s):  
L. G Israels ◽  
J Foerster ◽  
A Zipursky
Keyword(s):  
Vitamin A ◽  
Prothrombin Time ◽  
Marked Reduction ◽  
Factor Ix ◽  
Factor Vii ◽  
Factor V ◽  
Vitamin K1 ◽  
Hypervitaminosis A ◽  
Daily Feeding ◽  
Coagulation Defect

SummaryRats fed vitamin A, 70 000 u daily for a period of 28 days developed a hemorrhagic state characterized by a prolonged prothrombin time and stypven time, a marked reduction in prothrombin and the factor VII-complex, and an inconstant decrease in factor V activity. A serum defect in thromboplastin generation was also noted. The defects in the extrinsic system were prevented by the simultaneous daily feeding of 60 μg to 120 μg of vitamin K1 but this did not uniformly prevent the serum defect in thromboplastin generation which is thought to represent a depletion in factor IX.

Cloning and Characterization of the Murine Coagulation Factor X Gene

2000 ◽  
Vol 83 (05) ◽  
pp. 732-735 ◽  
Author(s):  
Adrian Cooper ◽  
Zhong Liang ◽  
Francis Castellino ◽  
Elliot Rosen
Keyword(s):  
Factor Viii ◽  
Coagulation Factor ◽  
Factor Ix ◽  
Coagulation Factor Viii ◽  
Start Codon ◽  
Factor Vii ◽  
Factor V ◽  
Factor X ◽  
Coagulation Factor Vii ◽  
Coagulation Factor V

SummaryThe gene encoding murine coagulation factor X (fX) was isolated and characterized from a λFIX II library generated from murine genomic DNA. The 20130 bp sequence contains 18049 nucleotides that extend from the initiating methionine to the polyadenylation site. 1056 nucleotides 5’ of the start codon were determined and contain putative start sites for the FX mRNA as well as sites for binding of putative transcription factors. The sequence extends 1024 3’ of the polyadenylattion site.The gene contains 8 exons and 7 introns which were determined by comparing the mouse FX cDNA and gene sequences. The exonic structure of the gene is similar to that of the other mammalian vitamin K-dependent serine proteases of the coagulation system. These include an exon encoding the prepropepetide, the gladomain, a short helical stack, two exons for the two EGF domains, the activation pepetide, and two exons encoding the serine protease domain. The 5’ sequence of the mouse FX gene overlaps with the 3’ region of the FVII gene indicating that the murine FVII and FX gene are arranged in a head to tail arrangement as they are in humans. Abbreviations: fVII, coagulation factor VII; fIX, coagulation factor IX; fX, coagulation factor X; PC, Protein C; fV, coagulation factor V; fVa, activated coagulation factor V; fVIII, coagulation factor VIII; fVIIIa, activated coagulation factor VIII.

Factor V Inhibitor Developing After Liver Transplantation in a 3-Year-Old Child

PEDIATRICS ◽  
1991 ◽  
Vol 88 (1) ◽  
pp. 156-159
Author(s):  
BRUCE GORDON ◽  
WILLIAM HAIRE ◽  
MICHAEL DUGGAN ◽  
ALAN LANGNAS ◽  
BYERS SHAW
Keyword(s):  
Liver Transplantation ◽  
Factor Viii ◽  
Prothrombin Time ◽  
Blood Coagulation ◽  
Partial Thromboplastin Time ◽  
Factor V ◽  
Bleeding Tendency ◽  
Normal Plasma ◽  
Surgical Operations

Acquired inhibitors of blood coagulation have been recognized with increasing frequency since the classic review by Margolius et al in 1961.1 The most common acquired inhibitor is directed against factor VIII and usually arises in patients with classical hemophilia.2 Inhibitors directed against factor V are considered rare; only 30 cases have been reported in the literature.3-6 The majority of these cases occur in patients olden than 60 years and many have arisen following major surgical operations. Patients present with variable bleeding tendency and a prolonged partial thromboplastin time (PTT) and prothrombin time (PT), which fail to correct with the addition of normal plasma.

Sign in / Sign up

Export Citation Format

Share Document