Blood coagulation as a cybernetic system: Control of autoprothrombin C (factor Xa) formation

Irwin, J. Foster; Seegers, Walter H.; Andary, Thomas J.; Fekete, Lajos; Novoa, Eduardo

doi:10.1016/0049-3848(75)90159-0

Cited by 16 publications

(4 citation statements)

References 23 publications

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“…is inactivated at a faster rate in a purified intrinsic system in the presence of factor X than in its absence. They also agree with a statement by Irwin et al (1975) concerning the effect of Auto C (factor Xa) on factor VIII. In view of these findings and in the absence of experimental details, it is difficult to explain the statement of Davie and Fujikawa (1975) in a review article that factor X a activates factor VIII.…”

Section: Discussionsupporting

confidence: 88%

Inactivation of Factor VIII by a Mechanism Independent of the Generation of Thrombin

Triantaphyllopoulos

1979

Thromb Haemost

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SummaryThrombin first activates and then inactivates factor VIII and for this reason thrombin has been considered responsible for the inactivation of factor VIII which occurs during clotting. Experiments described in this paper indicated that the activity of factor VIII is not reduced in factor IX or factor X deficient sera, while on the other hand this factor becomes inactivated in blood anticoagulated with high concentrations of hirudin which inhibit thrombin activity completely. This suggests that some other factor, besides thrombin, which is generated only in trace amounts in factor IX or factor X deficient plasmas, is also able to inactivate factor VIII. Purified factor X activated with insolubilized trypsin was added to purified preparations of factor VIII, which were free of both fibrinogen and prothrombin. Factor Xa was allowed to act for 5-60 minutes and then inactivated with phenylmethanesul- fonyl fluoride. Depending on the duration of the action of factor X a partial or complete inactivation of factor VIII was observed. This inactivation was also observed in the presence of hirudin, thus excluding the possibility that the effect was due to contamination with trace amounts of thrombin.

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Section: Discussionsupporting

confidence: 88%

Inactivation of Factor VIII by a Mechanism Independent of the Generation of Thrombin

Triantaphyllopoulos

1979

Thromb Haemost

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“…If the concentration of any single one is lowered, the yield of thrombin dimin ishes in direct proportion. We found the same to be true for the generation of Factor Xa in its five-com ponent system (Seegers, Irwin, Hillegas, Fekete andNovoa 1975, Irwin, Seegers, Andary, Fekete and. Factor IXa alone yielded a small amount of Factor Xa.…”

Section: Figsupporting

confidence: 61%

“…In this example, the concentration of Factor VIII was progres sively reduced. The initial velocity is extraordinarily high (Irwin, Seegers, Andary, Fekete and Novoa 1975).…”

Section: Figmentioning

confidence: 99%

VI. Factor X (Autoprothrombin III)

1981

Semin Thromb Hemost

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“…It has been postulated and generally accepted that coagulation occurs in a cybernetic manner with fibrin deposition and subsequent lysis occurring as a continuous process. 5,45,71,100 The manifestations of normal hemostasis versus increased fibrin deposition (thrombosis) or increased fibrino(geno)lysis (hemorrhage) depends upon a delicate balance between the procoagulant system and associated inhibitors, as well as the fibrino(geno)lytic system and its associated inhibitors. 38,66,73,99 Primary inhibitors of the procoagulant and fibrino(geno)lytic systems are comprised of antithrombin III, alpha 2macroglobulin, alpha 1 -antitrypsin, Cl esterase inhibitor, and alpha2-antiplasmin.…”

mentioning

confidence: 99%

Clinical Relevance of Antithrombin III

Bick¹

1982

Semin Thromb Hemost

141

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Many unrelated clinical conditions that are associated with significant decreases in antithrombin III have been summarized. In addition, prospects for future therapy with antithrombin III concentrates have been discussed. The clinical indications for antithrombin III determinations, including the reasons for performing the assay and those specific patient populations subjected to antithrombin III assays in this author's clinical practice, have been outlined. It is to be anticipated that with the new general availability of simple reliable antithrombin III assay systems using synthetic substrates that more and more populations will be adequately studied and clinical indications for the use of antithrombin III determinations and concentrates may become more firm or may change.

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Blood coagulation as a cybernetic system: Control of autoprothrombin C (factor Xa) formation

Cited by 16 publications

References 23 publications

Inactivation of Factor VIII by a Mechanism Independent of the Generation of Thrombin

Inactivation of Factor VIII by a Mechanism Independent of the Generation of Thrombin

VI. Factor X (Autoprothrombin III)

Clinical Relevance of Antithrombin III

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