Gel Filtration Properties of Factors II, VII, IX, IXa, and X

1972 ◽  
Vol 28 (02) ◽  
pp. 317-324 ◽  
Author(s):  
Bjarne Østerud ◽  
Sandra Schiffman
Keyword(s):  
Gel Filtration ◽  
Apparent Size ◽  
Factor Ix ◽  
Tris Buffer ◽  
Factor Vii ◽  
Factor Xii ◽  
Factor X ◽  
Clotting Factors ◽  
Filtration Properties ◽  
Plasma Factors

SummaryThe following gel filtration properties of the vitamin ढ dependent clotting factors have been established :1. The elution patterns of factors II, VII, IX, and X in 0.5 M NaCl are the same in factor XII deficient native plasma, anticoagulated plasma, and BaSO4 eluates.2. In 0.01 M Tris buffer pH 7.3 or 0.5 M NaCl, plasma factors II, IX, and X elute together; factor VII élûtes later as a smaller molecule. All 4 plasma activities elute as larger molecules in 0.01 M Tris buffer and smaller ones in 0.5 M NaCl.3. In 0.01 M Tris - 0.005 M EDTA peak factor II activity elutes first, followed by factor IX, factor X, and then factor VII.4. Activation decreases the apparent size of factor IX.

Very Low Activated Factor VII and Reduced Factor VII Antigen in Familial Abetalipoproteinaemia

1998 ◽  
Vol 80 (08) ◽  
pp. 233-238 ◽  
Author(s):  
K. A. Mitropoulos ◽  
M. N. Nanjee ◽  
D. J. Howarth ◽  
J. C. Martin ◽  
M. P. Esnouf ◽  
...  
Keyword(s):  
Plasma Concentrations ◽  
Positive Association ◽  
Factor Ix ◽  
Factor Vii ◽  
Unesterified Fatty Acid ◽  
Factor Xii ◽  
Factor X ◽  
Factor Xi ◽  
Activated Factor Vii ◽  
Normal Mean

SummaryAbetalipoproteinaemia is a rare disorder of apolipoprotein B metabolism associated with extremely low plasma concentrations of triglyce-ride. To discover whether the general positive association between factor VII and triglyceride levels extends to this condition, 5 patients were compared with 18 controls. All patients had a triglyceride below 100 μmol/l. Plasma unesterified fatty acid concentration was normal. Although factor IX activity was only slightly reduced (mean 88% standard) and factor IX antigen was normal, mean activated factor VII in patients was strikingly reduced to 34% of that in controls, a level similar to that found in haemophilia B. The patients’ mean factor VII activity and factor VII antigen were also significantly reduced to 54% and 63% of those in controls, respectively. Mean factor XI activity and tissue factor pathway inhibitor activity were reduced in patients to 70% and 75% of control values respectively, while factor XII, factor XI antigen, factor X, prothrombin and protein C were normal.

Neonatal Polycythemia: A Disorder Associated With Hyperviscosity, Normal Coagulation Findings And Thrombocytopenia

1981 ◽  
Author(s):  
J Katz ◽  
E Rodriguez ◽  
C Madani ◽  
D Hicks ◽  
H E Branson
Keyword(s):  
Plasma Exchange ◽  
Gestational Age ◽  
Degradation Products ◽  
Factor Ix ◽  
Factor Vii ◽  
Large For Gestational Age ◽  
Factor Xii ◽  
Factor X ◽  
Platelet Counts ◽  
Before And After

Thirty-two newborns with elevated capillary hematocrits >65% were studied. Twenty-two newborns required plasmaexchange transfusion. All had central (venous) hematocrits >65% and had symptoms referrable to complications associated with this syndrome. Of the 22, 15 were appropriate-for-gestational age, 5 were small-for-gestational age, and 2 were large-for-gestational age. Viscosity measurements in the 10 newborns who did not require plasma-exchanges showed increased viscosity in 2 in the slow shear rates associated with bloodflow in the smaller vessels. Coagulation data before and after plasma exchange did not show a hypercoagulable state: PT-14.2±0.7 and 12.9±1.2 secs, PTT 49.9±3.6 and 42.2±3.2 secs, factor VII 73±5 and 78±5%, factor VIII 103±10 and 94±10%, AT III levels were low 14±1.2 and 17±1.3 mg/dl, fibrin degradation products were <10μg/ml, fibrin monomer was not detected, plasminogen levels were 5±0.8 and 7±0.9mg/dl, fibrinogen levels were 203±9.8 and 200±11.8 mg%. Vitamin K dependent factors were reduced factor V 44±6 and 49±11%, factor VII 77±5 and 86±5%, factor IX 28±2 and 42±3%, factor X 35±4 and 62±6%, factor XI 55±5 and 84±9%, factor XII 47±5 and 63±5%. Statistical significant differences were found only with factors IX, X, XI and XII. Thrombocytopenia was present in 6 patients (20% incidence) and post plasma exchange the platelet counts rose significantly and in 2 patients within 3 days reached normal levels. No statistical difference in the platelet counts were noted before and after the plasma-exchange and were similar to the levels determined in 10 newborn controls. Neonatal polycythemia with thrombocytopenia may indicate a more severe disorder, with hematocrits in the 6 patients >70%. It is suggested that the mechanism of the thrombocytopenia may be aggregates of platelets that deaggregate following plasmaexchange. The complications associated with neonatal polycythemia appear related to hyperviscosity, erythrocyte and platelet “sludging” in the smaller vessels.

scholarly journals Coagulation Factor IX concentrate: method of preparation and assessment of potential in vivo thrombogenicity in animal models

Blood ◽  
1984 ◽  
Vol 64 (6) ◽  
pp. 1220-1227
Author(s):  
D Menache ◽  
HE Behre ◽  
CL Orthner ◽  
H Nunez ◽  
HD Anderson ◽  
...  
Keyword(s):  
Animal Models ◽  
Specific Activity ◽  
Rabbit Model ◽  
Coagulation Factor ◽  
Factor Ix ◽  
Factor Vii ◽  
Factor X ◽  
Clotting Factors ◽  
Coagulation Factor Ix

Thrombosis and/or disseminated intravascular coagulation (DIC) are complications specifically associated with the use of factor IX complex in some patients. Assuming that these complications might result from zymogen overload, we have produced, using diethylaminoethyl (DEAE)- Sephadex (Pharmacia, Piscataway, NJ) and sulfated dextran chromatography, a factor IX concentrate (coagulation factor IX) that is essentially free of prothrombin, factor VII, and factor X. Factor IX specific activity is at least 5 U/mg protein, a 250-fold purification compared to plasma. Amounts of factors II, VII, and X are less than 5 units each per 100 units of factor IX. The concentrate is essentially free of activated clotting factors and contains no added heparin. In the rabbit stasis model, a dose of 200 factor IX U/kg was less thrombogenic than 100 factor IX U/kg of the DEAE-Sephadex eluate from which the concentrate was derived. Infusion of 200 factor IX U/kg did not induce DIC in the nonstasis rabbit model, whereas 100 factor IX U/kg of the DEAE-Sephadex eluate resulted in DIC in this model. Several factor IX lots were found to have shortened nonactivated partial thromboplastin times (PTTs), but were nonthrombogenic in both animal models. These data indicate that coagulation factor IX concentrate is less thrombogenic than factor IX complex.

Intrauterine Subdural Hemorrhage Associated with Profound Deficiency of the Vitamin K Dependent Clotting Factors in an Infant Homozygous for a Common Polymorphism in the Vitamin K Epoxide Reductase Complex 1 (VKORC1) Promoter.

Blood ◽  
2007 ◽  
Vol 110 (11) ◽  
pp. 2152-2152
Author(s):  
Nadav Schwartz ◽  
Johannes Oldenburg ◽  
David Hart ◽  
Michael Nardi ◽  
Ori Langer Most ◽  
...  
Keyword(s):  
Vitamin K ◽  
Gestational Age ◽  
Subdural Hematoma ◽  
Factor Ix ◽  
Factor Vii ◽  
Dietary Vitamin ◽  
Subdural Hemorrhage ◽  
Factor X ◽  
Clotting Factors ◽  
Complete Sequencing

Abstract Hemorrhage in newborn infants who have not received vitamin K supplementation is a well recognized entity, but hemorrhage occurring prenatally due to deficiency of the vitamin K dependent factors is not. We report a subdural hemorrhage in a fetus at 29 weeks of gestation associated with very low levels of vitamin K dependent factors. The pregnancy was monitored by periodic ultrasound because of a previous near term stillbirth to this mother for which no etiology was identified. At 29 weeks a 4.6 × 7.7 × 8.8 cm left subdural hematoma was detected. There is no history of bleeding in this Hispanic family and no known consanguinity. His mother was not taking coumadin or any other medication, and her coagulation studies were normal. The baby was delivered by cesarean section, blood drawn for coagulation studies and 1mg Vitamin K given intramuscularly. The baby oozed from the injection and venipuncture sites. The hematocrit was 19% (mean for gestational age = 40.88) and packed red blood cells were given followed by fresh frozen plasma (10ml/kg). Platelets were 284,000/cmm. At six hours of life coagulation studies were greatly improved, the factor levels now being in the normal range for 29 weeks gestational age. Results at birth, 6 hours and 6 months are shown in the table. At 6 hours the baby no longer oozed from venipuncture sites. He received 1mg vitamin K daily for 3 days and no further supplementation thereafter other than that contained in infant formula. The subdural hematoma was drained on day 1 of life. Growth and development at 20 months are normal. Complete sequencing of the VKORC1 gene showed a homozygous functional promoter polymorphism: VKORC1:c.[1–1639&gt;A]+[1–1639&gt;A] (VKORC1*2/*2). This A allele is associated with 25% less VKORC1 expression and protein (50% less for homozygotes) compared to the G allele. Complete sequencing of the gamma-glutamyl carboxylase gene revealed no functional abnormalities. Individuals homozygous for this VKORC1 polymorphism have a relatively low capacity to regenerate reduced vitamin K and should require more vitamin K intake than others. They are known to require less warfarin. We hypothesize that insufficient vitamin K was available in utero to this fetus to compensate for the relatively low reductase level, and he became severely factor deficient. In the extra uterine environment sufficient dietary vitamin K was available to compensate for his relatively low reductase level. It is possible that the previous unexplained stillbirth was due to hemorrhage because of a similar factor deficiency. A reason for an intrauterine paucity of vitamin K has not been determined but must be rare as 17% of Europeans and a larger number of Chinese are homozygous VKORC1*2/*2, and intrauterine hemorrhage due to this cause is not reported. Birth 6 hours 6 months Values in parentheses are ELISA assays. Other assays are functional. nd = not done PT (sec) &gt;120 17.6 13.7 PTT (sec) 176 50.3 35.2 Fibrinogen (mg/dL) 194 196 287 % Factor II 1 39 96 % Factor V 81 nd 116 % Factor VII 3 61 99 % Factor IX 1 nd 108 % Factor X 2 (33) nd 107 % Protein C &lt;1 (18) 27 nd

scholarly journals Coagulation Factor IX concentrate: method of preparation and assessment of potential in vivo thrombogenicity in animal models

Blood ◽  
1984 ◽  
Vol 64 (6) ◽  
pp. 1220-1227 ◽  
Author(s):  
D Menache ◽  
HE Behre ◽  
CL Orthner ◽  
H Nunez ◽  
HD Anderson ◽  
...  
Keyword(s):  
Animal Models ◽  
Specific Activity ◽  
Rabbit Model ◽  
Coagulation Factor ◽  
Factor Ix ◽  
Factor Vii ◽  
Factor X ◽  
Clotting Factors ◽  
Coagulation Factor Ix

Abstract Thrombosis and/or disseminated intravascular coagulation (DIC) are complications specifically associated with the use of factor IX complex in some patients. Assuming that these complications might result from zymogen overload, we have produced, using diethylaminoethyl (DEAE)- Sephadex (Pharmacia, Piscataway, NJ) and sulfated dextran chromatography, a factor IX concentrate (coagulation factor IX) that is essentially free of prothrombin, factor VII, and factor X. Factor IX specific activity is at least 5 U/mg protein, a 250-fold purification compared to plasma. Amounts of factors II, VII, and X are less than 5 units each per 100 units of factor IX. The concentrate is essentially free of activated clotting factors and contains no added heparin. In the rabbit stasis model, a dose of 200 factor IX U/kg was less thrombogenic than 100 factor IX U/kg of the DEAE-Sephadex eluate from which the concentrate was derived. Infusion of 200 factor IX U/kg did not induce DIC in the nonstasis rabbit model, whereas 100 factor IX U/kg of the DEAE-Sephadex eluate resulted in DIC in this model. Several factor IX lots were found to have shortened nonactivated partial thromboplastin times (PTTs), but were nonthrombogenic in both animal models. These data indicate that coagulation factor IX concentrate is less thrombogenic than factor IX complex.

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 Activation of human factor VII in the initiation of tissue factor- dependent coagulation

Blood ◽  
1986 ◽  
Vol 68 (3) ◽  
pp. 685-691 ◽  
Author(s):  
LV Rao ◽  
SI Rapaport ◽  
SP Bajaj
Keyword(s):  
Tissue Factor ◽  
Factor Ix ◽  
Factor Vii ◽  
Activate Factor ◽  
Factor Xii ◽  
Factor X ◽  
Clotting Time ◽  
Activated Factor Vii ◽  
Peptide Release ◽  
Minimal Generation

Abstract We have used activation peptide release assays to compare factor VII and activated factor VII (VIIa) activation of factor X, normal factor IX (IXN), and a variant factor IX (IXBmLE), which, after activation, is unable to back-activate factor VII. In purified systems, factor VII and VIIa each rapidly activated factor X, but after a one minute lag for factor VII. VIIa also readily activated both IXN and IXBmLE. Factor VII initially failed to activate substantial amounts of either IXN or IXBmLE; on further incubation factor VII activated IXN but not IXBmLE. Activation of IXN began when approximately 10% of factor VII had been converted to VIIa, as measured by 125I-factor VII radioactivity profiles. Adding factor VII to VIIa slowed its activation of IXBmLE. However, in the presence of factor X, factor VII alone rapidly activated IXBmLE. Unlike purified systems, 1 nmol/L VIIa added to factor VII-deficient plasma failed to activate factor IX. Increasing factor VII to 10 nmol/L (plasma concentration) either as native VII or VIIa yielded similar activation curves for factor IX and similar activation curves for factor X. Adding 5% VIIa to factor X-deficient plasma and to factor XII-deficient plasma substantially shortened the dilute tissue factor clotting time of only the former. These data support the hypothesis that factor VII/tissue factor complex initiates tissue factor-dependent clotting through a minimal generation of Xa. This Xa then rapidly back-activates a small amount of factor VII, following which the rates of activation of both factors IX and X increase dramatically.

scholarly journals Puerarin Attenuates Ovalbumin-Induced Lung Inflammation and Hemostatic Unbalance in Rat Asthma Model

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Feng Dong ◽  
Chengbin Wang ◽  
Jinyan Duan ◽  
Weiyi Zhang ◽  
Daijun Xiang ◽  
...  
Keyword(s):  
Lung Tissue ◽  
Factor Ix ◽  
Allergic Airway Disease ◽  
Factor Vii ◽  
Tissue Homogenate ◽  
Coagulation Disorder ◽  
Factor Xii ◽  
Thrombin Time ◽  
Factor X ◽  
Cell Counts

Aim.We aimed to investigate and evaluate the preventive activity of puerarin on the ovalbumin-induced asthma rat model.Materials and Methods.Male Wistar rats were sensitized intraperitoneally on days 0, 7, and 14 and challenged to ovalbumin intratracheally on day 21. Groups of sensitized rats were treated randomly either with placebo, puerarin, dexamethasone, or puerarin combined with dexamethasone, from days 15 to 20. Inflammatory markers, including cell counts in bronchoalveolar lavage fluid (BALF), inflammatory cytokines, histopathology, and coagulation parameters, such as coagulation tests and the activity of coagulation factors, were analyzed.Results.Puerarin significantly inhibited the recruitment of inflammatory cells in BALF and lung tissue. At the same time, the release of IL-4, IL-10, and IFN-γin serum and the expression of mRNAs in lung tissue homogenate were changed by puerarin. Administration of puerarin also effectively rectified the coagulation disorder in asthmatic rats, such as prothrombin time (PT) (P<0.01), thrombin time (TT) (P<0.05), fibrinogen (FIB) (P<0.01),the activity of factor II (FII) (P<0.01), the activity of factor V (FV) (P<0.05), the activity of factor VII (FVII) (P<0.05), the activity of factor X (FX) (P<0.05), the activity of factor VIII (FVIII) (P<0.01), the activity of factor IX (FIX) (P<0.05), and the activity of factor XII (FXII) (P<0.05).Conclusions.Our results provide a clue that puerarin was useful for the preventive of allergic airway disease in rodents.

scholarly journals Activation of human factor VII in the initiation of tissue factor- dependent coagulation

Blood ◽  
1986 ◽  
Vol 68 (3) ◽  
pp. 685-691 ◽  
Author(s):  
LV Rao ◽  
SI Rapaport ◽  
SP Bajaj
Keyword(s):  
Tissue Factor ◽  
Factor Ix ◽  
Factor Vii ◽  
Activate Factor ◽  
Factor Xii ◽  
Factor X ◽  
Clotting Time ◽  
Activated Factor Vii ◽  
Peptide Release ◽  
Minimal Generation

We have used activation peptide release assays to compare factor VII and activated factor VII (VIIa) activation of factor X, normal factor IX (IXN), and a variant factor IX (IXBmLE), which, after activation, is unable to back-activate factor VII. In purified systems, factor VII and VIIa each rapidly activated factor X, but after a one minute lag for factor VII. VIIa also readily activated both IXN and IXBmLE. Factor VII initially failed to activate substantial amounts of either IXN or IXBmLE; on further incubation factor VII activated IXN but not IXBmLE. Activation of IXN began when approximately 10% of factor VII had been converted to VIIa, as measured by 125I-factor VII radioactivity profiles. Adding factor VII to VIIa slowed its activation of IXBmLE. However, in the presence of factor X, factor VII alone rapidly activated IXBmLE. Unlike purified systems, 1 nmol/L VIIa added to factor VII-deficient plasma failed to activate factor IX. Increasing factor VII to 10 nmol/L (plasma concentration) either as native VII or VIIa yielded similar activation curves for factor IX and similar activation curves for factor X. Adding 5% VIIa to factor X-deficient plasma and to factor XII-deficient plasma substantially shortened the dilute tissue factor clotting time of only the former. These data support the hypothesis that factor VII/tissue factor complex initiates tissue factor-dependent clotting through a minimal generation of Xa. This Xa then rapidly back-activates a small amount of factor VII, following which the rates of activation of both factors IX and X increase dramatically.

A Distinction between the Role of Precursor and Activated Forms of Clotting Factors in the Genesis of Stasis Thrombi

1967 ◽  
Vol 18 (01/02) ◽  
pp. 012-023 ◽  
Author(s):  
S Wessler ◽  
E. T Yin ◽  
L. W Gaston ◽  
Iona Nicol
Keyword(s):  
Human Serum ◽  
Factor Ix ◽  
In Vivo Studies ◽  
Factor Vii ◽  
Factor X ◽  
Clotting Factors ◽  
Insight Into

Summary1. In vivo studies in rabbits have shown that the liver diminishes the thrombo-genicity of infused human serum.2. In vitro rabbit liver perfusions with human serum have demonstrated the loss of serum thrombogenicity within 5 min after the onset of the perfusion. Associated with this loss of thrombotic capacity is a marked decrease in the activation product (AP) and labile factor IX (PPA) activity in the infused serum.3. The liver appears to have the capacity to discriminate between circulating activated clotting activities such as AP and PPA and inactive procoagulants such as stable or genuine factor IX, factor VII and factor X. The latter are not cleared from the circulation by the liver.4. These studies provide some insight into the mechanism whereby circulating activated clotting activities and retarded blood flow predispose to thrombosis.

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