Development of Increased Factor Vii Activity During the Spontaneous Coagulation of Blood

Johnston, Charles G.; Hjort, Peter Fredrik

doi:10.1172/jci104308

Cited by 22 publications

(8 citation statements)

References 8 publications

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“…This suggests to us that Factor IXa was the principal activator of Factor VII under these experimental conditions. The activation of Factor VII found after clotting of Factor Xdeficient plasma confirms earlier observations of Hougie (27) and of Johnston and Hjort (2).…”

Section: Purified 8-xiia Was Much More Effective In Activatingsupporting

confidence: 90%

“…Furthermore, Factor VII activity increased when kallikrein was added either to Factor XII-deficient plasma or to Factor IX-deficient plasma. Our (2) that Factor VII was activated after clotting of blood from patients with extreme thrombocytopenia. It should also be pointed out that in some of our experiments with antisera, Factor VII was activated by Factor IXa in the absence of added calcium ions.…”

Section: Purified 8-xiia Was Much More Effective In Activatingmentioning

confidence: 76%

“…Factor VII activity, as measured in one-stage Factor VII clotting assays (1), increases several fold when blood is exposed to a surface such as glass or kaolin (1), or when blood is allowed to clot (2). Factor VII activity also increases when plasma from women taking oral contraceptives is stored at 4°C (3).…”

Section: Introductionmentioning

confidence: 99%

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Activation of Human Factor VII in Plasma and in Purified Systems

Seligsohn¹,

Østerud²,

Brown³

et al. 1979

J. Clin. Invest.

158

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A B S T R A C T Factor VII can be activated, to a molecule giving shorter clotting times with tissue factor, by incubating plasma with kaolin or by clotting plasma. The mechanisms of activation differ. With kaolin, activated Factor XII (XIIa) was the apparent principal activator. Thus, Factor VII was not activated in Factor XII-deficient plasma, was partially activated in prekallikrein and high-molecular weight kininogen (HMW kininogen)-deficient plasmas, but was activated in other deficient plasmas. After clotting, activated Factor IX (IXa) was the apparent principal activator. Thus, Factor VII was not activated in Factor XII-, HMW kininogen-, XI-, and IX-deficient plasmas, but was activated in Factor VIII-, X-, and V-deficient plasmas. In further studies, purified small-fragment Factor XIIa (,8-XIIa), kallikrein, and Factor IXa were added to partially purified Factor VII and to plasma.

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Section: Purified 8-xiia Was Much More Effective In Activatingsupporting

confidence: 90%

Section: Purified 8-xiia Was Much More Effective In Activatingmentioning

confidence: 76%

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Activation of Human Factor VII in Plasma and in Purified Systems

Seligsohn¹,

Østerud²,

Brown³

et al. 1979

J. Clin. Invest.

158

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“…High levels of F VII Ag were found in "compensated" DIC (normal or slightly decreased platelet count and fibrinogen levels) associated with consistently higher levels of F VII C (ratio of F VII C to F VII Ag close to 1.35). These results are probably related ,to the presence of activated F VII, as suggested by others (32)(33)(34). In contrast, in "decompensated" DIC (low fibrinogen and platelet count), F VII was markedly reduced, with a good correlation between F VII Ag and F VII C.…”

Section: Discussionsupporting

confidence: 74%

An Enzyme Immunoassay (ELISA) for the Quantitation of Human Factor VII

et al. 1986

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SummaryA new solid phase enzyme-linked immunosorbent assay (ELISA) was developed for the quantitation of human Factor VII antigen (F VII Ag), using a monospecific rabbit anti-F VII antiserum. Anti-F VII F(ab′)2 fragments were adsorbed to polystyrene plates. The binding of serial dilutions of control or test plasma, containing F VII, was detected by incubation with peroxidase-labeled anti- FV II IgG followed by the addition of hydrogen peroxyde and O-phenylenediamine. This ELISA is specific, sensitive (detection limit: 0.05%) and accurate (coefficient of variation: 1.5-4% for within- and 1.6-9% for between-assays). F VII coagulant activity (F VII C) and F VII Ag were determined in large populations of controls and patients. In normal plasma (n = 38), F VII Ag ranged from 83 to 117% and the correlation coefficient between F VII Ag and F VII C was 0.94. In patients with severe (F VII C inf. 1%) congenital F VII deficiency (n = 5), F VII Ag was undetectable in two cases (inf. 0.05%) and markedly reduced (0.35 to 5.6%) in the three other cases. In patients with liver cirrhosis (n = 15), F VII Ag ranged from 21 to 59% and was in good correlation with F VII C (r = 0.84). In dicoumarol treated patients (n = 15), the levels of F VII Ag ranged from 51% to 79% and a poor correlation (r = 0.52) with F VIIC was observed. In “compensated” DIC (n = 5), levels of F VII Ag varied from 60 to 186%, with significantly higher F VII C levels (from 143 to 189%). In contrast, in “decompensated” DIC (n = 7), low F VII Ag and F VII C levels were observed (from 7 to 27%). In patients with deep-vein thrombosis (n = 25), high levels of F VII Ag (from 102 to 136%) and F VII C (from 110 to 150%) were demonstrated. In surgical patients, no significant difference was observed before and one day after intervention.

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“…Factor VII is activated when blood clots in vitro, with or without tissue thromboplastin (Johnston & Hjort 1961), and serum may appear to possess three to four times the Factor VII activity of the original plasma. Therefore, we assume that some Factor VII was also activated during intravascular clotting in our animals.…”

Section: Discuss I 0 Nmentioning

confidence: 99%

Consumption of Serum Factors and Prothrombin During Intravascular Clotting in Rabbits

Rapaport

Hjort

Patch

et al. 1966

Scandinavian Journal of Haematology

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We have studied the effect of experimental intravascular clotting upon Factors II, VII, IX, and X in rabbits. Animals were given sodium warfarin intravenously to block the synthesis of these factors and, 4 hours later, were infused with either dilute tissue thromboplastin or saline. The tissue thromboplastin induced intravascular clotting extensive enough to halve fibrinogen and platelet levels and to reduce markedly Factor V and Factor VIII levels. These changes resulted from a consumption during clotting of about 10 per cent of the available prothrombin. Each of the serum factors fell further during the infusion of tissue thromboplastin than during the infusion of saline; apparently, serum factors activated during clotting do not circulate in the rabbit. Net losses due to intravascular clotting equalled about 15 to 30 per cent of the Factors VII, IX, and X initially present. These data suggest that consumption during intravascular clotting may account for the low levels of Factors VII, IX, and X described in patients with diffuse intravascular clotting complicating septicaemia. The evidence of consumption of Factor IX raises the possibility that tissue thromboplastin may activate intrinsic clotting during hemostasis in vivo.

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Development of Increased Factor Vii Activity During the Spontaneous Coagulation of Blood

Cited by 22 publications

References 8 publications

Activation of Human Factor VII in Plasma and in Purified Systems

Activation of Human Factor VII in Plasma and in Purified Systems

An Enzyme Immunoassay (ELISA) for the Quantitation of Human Factor VII

Consumption of Serum Factors and Prothrombin During Intravascular Clotting in Rabbits

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