ANTICOAGULANT EFFECT OF INCUBATED FIBRINOGEN

1958 ◽  
Vol 36 (1) ◽  
pp. 249-259 ◽  
Author(s):  
D. C. Triantaphyllopoulos
Keyword(s):  
Ammonium Sulphate ◽  
Coagulation Factors ◽  
The Other ◽  
Anticoagulant Effect ◽  
Factor Vii ◽  
Factor V ◽  
Thrombin Time ◽  
Fresh Plasma ◽  
Native Plasma ◽  
Ammonium Sulphate Saturation

Sterile fibrinogen rendered non-clottable by incubation was mixed with fresh plasma and the thrombin time determined. An appreciable prolongation was observed. The incubated fibrinogen was then fractionally precipitated with ammonium sulphate. The material precipitated between 25 and 50% ammonium sulphate saturation, when added to freshly drawn but still unclotted blood, or native plasma, prevented its coagulation. This action could be reversed by an approximately fivefold dilution with distilled water and addition of calcium chloride and thrombin, thus excluding fibrinolysis as the cause of the anticoagulant effect. Determinations of the respective coagulation factors showed that no decrease occurred in prothrombin, factor VII, plasma thromboplastin component, and fibrinogen. On the other hand a statistically significant decrease in factor V was observed when calcium was present.

ANTICOAGULANT EFFECT OF INCUBATED FIBRINOGEN

1958 ◽  
Vol 36 (3) ◽  
pp. 249-259 ◽  
Author(s):  
D. C. Triantaphyllopoulos
Keyword(s):  
Ammonium Sulphate ◽  
Coagulation Factors ◽  
The Other ◽  
Anticoagulant Effect ◽  
Factor Vii ◽  
Factor V ◽  
Thrombin Time ◽  
Fresh Plasma ◽  
Native Plasma ◽  
Ammonium Sulphate Saturation

Sterile fibrinogen rendered non-clottable by incubation was mixed with fresh plasma and the thrombin time determined. An appreciable prolongation was observed. The incubated fibrinogen was then fractionally precipitated with ammonium sulphate. The material precipitated between 25 and 50% ammonium sulphate saturation, when added to freshly drawn but still unclotted blood, or native plasma, prevented its coagulation. This action could be reversed by an approximately fivefold dilution with distilled water and addition of calcium chloride and thrombin, thus excluding fibrinolysis as the cause of the anticoagulant effect. Determinations of the respective coagulation factors showed that no decrease occurred in prothrombin, factor VII, plasma thromboplastin component, and fibrinogen. On the other hand a statistically significant decrease in factor V was observed when calcium was present.

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.

Changes Occurring During Coagulation in Glass. I. Normal Human Blood

1960 ◽  
Vol 4 (01) ◽  
pp. 001-016
Author(s):  
Jessica H. Lewis ◽  
Paul Didisheim ◽  
John H. Ferguson ◽  
Kenichi Hattori
Keyword(s):  
Coagulation Factors ◽  
Factor Ix ◽  
Factor Vii ◽  
Sodium Oxalate ◽  
Factor V ◽  
Rapid Rise ◽  
Rapid Fall ◽  
Glass Tubes ◽  
Normal Human ◽  
The Individual

SummaryNormal whole blood was allowed to stand in glass tubes at 37° C, and the clotting process stopped at various intervals by the addition of sodium oxalate. During the first 15 minutes a marked acceleration of clotting activity was found. Study of the individual coagulation factors showed the following changes: a sustained and rapid fall in platelet count, a sustained and rapid rise in PTC (factor IX), a steady fall in fibrinogen, a more gradual fall in AHF (factor VIII), a rapid rise and subsequent fall in proaccelerin (factor V) activity, a somewhat lesser and slower rise and fall in proconvertin (factor VII) activity, and a slow fall in prothrombin concentration. No changes were noted in Hageman factor or PTA activities.

FACTOR II ACTIVATING ACTIVITY IN EXTRACTS OF TUMORAL NECROSIS FROM TWO MURINE BREAST ADENOCARCINOMAS

1987 ◽  
Author(s):  
A Blanco ◽  
R Bonfil ◽  
O Bustoabad ◽  
M Lazzari
Keyword(s):  
Coagulation Factors ◽  
Factor Vii ◽  
Factor V ◽  
Factor X ◽  
Extrinsic Pathway ◽  
Factor Ii ◽  
Metastatic Capacity ◽  
Plasma Recalcification Time ◽  
Recalcification Time ◽  
Breast Adenocarcinomas

Increased deposition and lysis of fibrin, associated with malignant tissue, has led to look for activators of both the coagulation and fibrinolytic systems produced by tumor cells. We report the evidences of a procoagblant activity (PA) in the extracts of intratumoral necrosis from two experimental breast adenocarcinomas in murine model (BALB/c). The tumors have different metastatic capacity (MC). M3 without MC and MM3 with high MC.The addition of the extracts to: 1- Normal Plasma, 2- Deficient substrates in coagulation factors, 3- Purified, fibrinogen (I), showed: 1- Shortening of the plasma recalcification time (PRT) and APTT, without ;modification on prothrombin time (PT), 2- Reduction of the PRT on deficient substrates in factors: VIII; VII; VII and X; V; V, VII and X; without modification on II deficient substrate, 3- No PA on I. Table:C: Control, s: seconds, m: minutes. The PA was not affected by heparin. The results suggest that the PA is independent of the presence of either factor VIII or factor VII (intrinsic or extrinsic pathway respectively), as well as presence of either factor V or factor X. Any effect was observed either on factor II deficient substrate or on I, so, there was no evidence of thrombin activity The PA could be act directly on factor II, suggesting that fibrin formation could be induced by a “non-classical” activation pathway. No significant differences (p>0.5) in PA were observed between both tumoral necrosis extracts. The necrotic area in M3 (37%) is bigger than in MM3 (18%). So, much more PA could be present in MM3 and this could play a role in the MC of this tumor.

scholarly journals Parahaemophilia: A Rare Case Report

2020 ◽  
Vol 38 (4) ◽  
pp. 205-208
Author(s):  
Mohammed Nuruzzaman Bhuiyan ◽  
Susane Giti ◽  
Arif Ahmed Khan ◽  
Md Moshiur Rahman ◽  
Md Anwarul Karim
Keyword(s):  
Rare Case ◽  
Bleeding Time ◽  
Armed Forces ◽  
Coagulation Factors ◽  
Activated Partial Thromboplastin Time ◽  
Factor V ◽  
Thrombin Time ◽  
Normal Range ◽  
Rare Case Report ◽  
Mucosal Bleeding

Parahaemophilia or Owren’s diseaseis a rare haemorrhagic disorder occurs due to congenital and frequently familial deficiency of Factor V.It is characterized by epistaxis, bruising, mucosal bleeding, soft tissue bleeding and haemarthrosis. We report a case of 6 year old female patient with overlapping features with other haemorrhagic disorder. With the complaints of recurrent episodic per rectal bleeding, patient was evaluated at different hospitals in Chattagram and was diagnosed as a case of Haemophilia B and treated accordingly. As her condition was not improved expectedly, she was referred to Armed Forces Institute of Pathology (AFIP) for further evaluation. The lab tests showed prolongation of prothrombin time (PT) and activated partial thromboplastin time (APTT), with normal bleeding time (BT) and thrombin time (TT). Coagulation factors assay revealed a significant decrease of factor V, 1% of normal range. Other coagulation factors are normal. She was treated with FFP and recovered four weeks after treatment. J Bangladesh Coll Phys Surg 2020; 38(4): 205-208

The Fractionation of Factor V from Human Plasma

1974 ◽  
Vol 31 (03) ◽  
pp. 457-468 ◽  
Author(s):  
John C. Giddings
Keyword(s):  
Human Plasma ◽  
Gel Electrophoresis ◽  
Chloride Solution ◽  
Specific Activity ◽  
Polyacrylamide Gel Electrophoresis ◽  
Coagulation Factors ◽  
Polycythaemia Vera ◽  
Agarose Gel ◽  
Factor V ◽  
Fresh Plasma

SummaryHuman plasma from normal donors and from patients with polycythaemia vera was fractionated in order to obtain a preparation of highly purified factor V. Fresh plasma was initially treated with aluminium hydroxide to remove factors II, VII, IX and X. Fibrinogen, factor VIII and most of the immunoglobulins were removed by precipitation with ethanol at -5° C. Crude factor V was precipitated with dilute acetic acid at pH 5.1, and then further purified by precipitation with acridine lactate (Rivanol), extraction with sodium chloride solution and column chromatography on agarose gel. Factor V was purified four hundred times with specific activity of 2.5-6.0 units per mg. protein. The final concentrate was devoid of activity of other coagulation factors but was heterogeneous on disc Polyacrylamide gel electrophoresis and Immunoelectrophoresis against anti human serum. On rechromatography on agarose gel there was a single peak of factor V activity, the molecular weight of which was estimated to be 300,000.

Changes with age in Fibrinolytic Activity, Coagulation Factors and Lipids in an Industrial Population

1975 ◽  
Author(s):  
R. Chakrabarti ◽  
M. Brozovic ◽  
T. W. Meade ◽  
W. R. S. North ◽  
Y. Stirling
Keyword(s):  
Fibrinolytic Activity ◽  
Blood Clot ◽  
Coagulation Factors ◽  
Blood Cholesterol ◽  
Factor Vii ◽  
Clot Lysis ◽  
Factor V ◽  
Cholesterol Levels ◽  
Lysis Time ◽  
Similar Factor

Fibrinolytic activity, coagulation factors I, V, VII and VIII, blood cholesterol and triglyceride levels have been measured in a randomyl selected group of 650 men aged 17–64 and 350 women aged 17–59 working in an industrial population. Fibrinolytic activity (the reciprocal of the dilute blood clot lysis time in hours) decreases significantly (0.003 per annum) with advancing age in men; there is no significant change in women. Factors I and V increase significantly with age in both men and women at about the same rate (1.0% per annum for factor I and 0.6% for factor V), their mean levels in each group being very similar. Factor VIII also increases significantly with age in both sexes up to the age of about 50 years, after which levels continue to rise in men, but fall in women. Factor VII and blood cholesterol levels are lower in young women than in young men; they rise in both sexes, but significantly faster in women than in men (1.1% and 0.4%, respectively for factor VII, for example), so that in older women they are substantially higher than in older men. Triglyceride levels rise with age in both sexes, levels in men being hig er than those in women.

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.

A New Fibrinogen Anomaly: Fibrinogen Buenos Aires

1975 ◽  
Author(s):  
J. A. Buraschi ◽  
E. S. Sack ◽  
E. Quiroga ◽  
H. Hendler
Keyword(s):  
Plasma Polymerization ◽  
Buenos Aires ◽  
Coagulation Factors ◽  
Thrombin Time ◽  
Clot Retraction ◽  
Bovine Thrombin ◽  
Hemorrhagic Tendency ◽  
Fresh Plasma ◽  
Antithrombin Iii Activity ◽  
Fibrin Monomers

Report of a familial defect of fibrinogen in a 42 year old woman and in one of her siblings. The defect in the boy produced different abnormalities. She had a lifelong hemorrhagic tendency and deffective wound healing and only slight prolongation of the thrombin time. She had normal fibrinogen levels (tested by several methods) and normal coagulation factors (including Factor XIII). Both fibrinolytic mechanism and platelet function were normal. Plasmatic antithrombin III activity was normal whereas its serum activity was increased. The bleeding time was moderately prolonged and clot retraction impaired. The thromboelastogram showed reduction of the “ma.” and plasma polymerization was deficient. These last two abnormalities were partially corrected by transfusions of fresh plasma. Aggregation of fibrin monomers was also deficient whereas fibrinopeptide release was quantitatively normal. The abnormal fibrinogen has increased immunoelectrophoretic mobility and an abnormal sedimentation pattern.Her son had a markedly prolonged thrombin time with bovine thrombin whereas with the human enzyme the test was moderately abnormal. Plasma polymerization was absent and sedimentation cooefficient increased. Reptilase time was normal. The abnormal fibrinogen is tentatively designated fibrinogen Buenos Aires, since its possible identity with other abnormal fibrinogen has not been excluded.

EFFECTS OF INTRAVENOUS INJECTIONS OF THE ANTICOAGULANT FRACTION OF INCUBATED FIBRINOGEN ON BLOOD COAGULATION

1960 ◽  
Vol 38 (1) ◽  
pp. 909-918 ◽  
Author(s):  
D. C. Triantaphyllopoulos
Keyword(s):  
Prothrombin Time ◽  
Bleeding Time ◽  
Jugular Vein ◽  
Coagulation Factors ◽  
External Jugular Vein ◽  
Anticoagulant Effect ◽  
Clotting Time ◽  
Intravenous Injections ◽  
Fibrinogen Content ◽  
Ammonium Sulphate Saturation

AFIF (Anticoagulant Fraction of Incubated Fibrinogen precipitated between 25 and 50% ammonium sulphate saturation) prepared from Armour's incubated bovine fibrinogen was injected in a dosage of 46–106 mg (mean: 66.5 mg) tyrosine per kilogram body weight in the external jugular vein of 10 rabbits. Blood samples were withdrawn at [Formula: see text]- or 1-hour intervals until the aspirated blood began showing signs of coagulation. The anticoagulant effect was manifested immediately and lasted for [Formula: see text] to [Formula: see text] hours in the animal. Although the blood aspirated during this time remained unclotted even after 24 hours, the surgical wound in the neck of the animal did not bleed and autopsies revealed no sign of internal haemorrhage. The bleeding time, however, was found prolonged when tested by cutting the marginal vein of the ear. The level of the coagulation factors was determined both in oxalated specimens and in specimens with no anticoagulant added. Both kinds of sample showed: (1) clottable fibrinogen content normal, thus excluding fibrinolysis as the cause of the anticoagulant effect; (2) thrombin clotting time of infinity; (3) one-stage prothrombin time longer than 60 seconds; (4) no correction of the infinite thrombin clotting time of oxalated specimens following the addition of 0.25 mg protamine per ml. This makes unlikely any appreciable release of heparin by the animal. However, oxalated and non-oxalated specimens differed in the following respects: (1) prothrombin time determined after adsorption and mixing of the eluate with adsorbed plasma was found to be normal for the oxalated blood but variably increased for the non-oxalated specimen (10–34.5 seconds); (2) the plasma precursors of plasma thromboplastin were normal in oxalated but very low in native specimens. The serum precursors of plasma thromboplastin were normal.

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