Thromb Haemost 1959; 03(03): 367-374
DOI: 10.1055/s-0038-1654397
Originalarbeiten — Original Articles — Travaux Originaux
Schattauer GmbH

The Fate of Factor VII and Stuart Factor During the Clotting of Normal Blood [*)]

Charles L Johnston jr.
1   Department of Physiology, University of North Carolina School of Medicine, Chapel Hill, N. C, USA
,
John H Ferguson
1   Department of Physiology, University of North Carolina School of Medicine, Chapel Hill, N. C, USA
,
Frieda A O’Hanlon
1   Department of Physiology, University of North Carolina School of Medicine, Chapel Hill, N. C, USA
,
W. L Black
1   Department of Physiology, University of North Carolina School of Medicine, Chapel Hill, N. C, USA
› Author Affiliations
Further Information

Publication History

Publication Date:
08 June 2018 (online)

Summary

Studies have been presented, utilizing factor specific assays, to show that Factor VII and Stuart factor behave differently during the clotting of normal blood. Stuart factor was neither consumed nor activated during clotting. In contrast, Factor VII was “activated” so that serum contained 2V2 to 3 times the plasma concentration of the factor. Marked rate changes occurred in the Factor VII activation curves when the sample incubation temperature was changed. The data obtained suggested that the optimum temperature for Factor VII activation may be at or near 18° C. Previous “consumption” data for “Factor VII” obtained by assays sensitive to changes in both Stuart factor and Factor VII have been validated, since the concentration of Stuart factor does not change during clotting.

*) This investigation was supported by Research Grant H-1510 (C5), National Institutes of Health.


 
  • References

  • 1 Hougie C, Barrow E. M, Graham J. B. Stuart Clotting Defect. I. Segregation of an hereditary hemorrhagic state from the heterogenous group heretofore called "Stable Factor" (SPCA, Proconvertin, Factor VII) deficiency. J. clin. Invest 1957; 36: 485
  • 2 Lewis J. H, Fresh J. W, Ferguson J. H. Congenital Hypoproconvertinemia. Proc. Soc. exp. Biol. (N. Y) 1953; 84: 651
  • 3 Alexander B, Goldstein R, Landwehr G, Cook C. D. Congenital SPCA-Deficiency: A hitherto unrecognized coagulation defect with hemorrhage rectified by serum and serum fractions. J. clin. Invest 1951; 30: 596
  • 4 Bachmann F, Duckert F, Geiger M, Baer P, Koller F. Differentiation of the Factor VII Complex. Studies on the Stuart-Prower Factor. Thromb. Diath. haem 1957; 1: 169
  • 5 Rodman jr. N. F, Barrow E. M, Graham J. B. Diagnosis and Control of the Hemophiloid States with the Partial Thromboplastin Time (PTT) Test. Amer. J. clin. Path 1958; 29: 525
  • 6 Ware A. G, Seegers W. H. Two Stage Procedure for the Quantitative Determination of Prothrombin Concentration. Amer. J. clin. Path 1949; 19: 471
  • 7 Lewis J. H, Ferguson J. H, Fresh J. W, Zucker M. B. Primary Hemorrhagic Disease. J. Lab. clin. Med 1957; 49: 216
  • 8 Ferguson J. H, Johnston jr. C. L, Howell D. A. A Circulating-Inhibitor (Anti-AcG) Specific for the Labile Factor-V of the Blood-Clotting Mechanism. Bloo 1958; 13: 382
  • 9 Sise H. S, Lavelle S. M, Becker R. A Method for Assay of Stuart Factor. Proc. Soc. exp. Biol (N. Y.) 1957; 96: 662
  • 10 Bachmann F, Duckert F, Koller F. The Stuart-Prower Factor Assay and its Clinical Significance. Thromb. Diath. haem 1958; 2: 2
  • 11 Fell C, Johnson J. F, Seegers W. H. Effect of Seitz Filtration on Plasma Trace Proteins Concerned with Blood Coagulation. Amer. J. clin. Path 1954; 24: 153
  • 12 Johnston jr. C. L, Ferguson J. H, O’Hanlon F. A. Surface Activation of Plasma Clotting: A function of Hageman Factor. Proc. Soc. exp. Biol. (N. Y) 1958; 99: 197
  • 13 Owren P. A. New Clotting Factors. Trans. 5th Conf. Blood Clotting and Allied Problems. Josiah Macy, jr. Foundation: New York; 1952: p. 92