Thromb Haemost 1961; 6(01): 025-036
DOI: 10.1055/s-0038-1654536
Originalarbeiten — Original Articles — Travaux Originaux
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Pulmonary Embolization in the Dog: Its Effects on Blood Coagulation and on Pulmonary Artery Pressures[*]

James W. Hampton M.D.
1   Departments of Medicine and Pathology, University of Oklahoma School of Medicine, Oklahoma City, Oklahoma
,
William E. Jaques M.D.
1   Departments of Medicine and Pathology, University of Oklahoma School of Medicine, Oklahoma City, Oklahoma
,
Robert M. Bird M.D.
1   Departments of Medicine and Pathology, University of Oklahoma School of Medicine, Oklahoma City, Oklahoma
,
David M. Selby B.S.
1   Departments of Medicine and Pathology, University of Oklahoma School of Medicine, Oklahoma City, Oklahoma
› Author Affiliations
This investigation was supported by U. S. Public Health Service training grant 2A—5107, National Institute of Arthritis and Metabolic Diseases, and by research grants H-3235 and H-3486, National Heart Institute.
Further Information

Publication History

Publication Date:
12 July 2018 (online)

Summary

1. Infusions containing particulate matter, viz. whole amniotic fluid, amniotic fluid sediment, and glass beads, produce in dogs changes in both early and late phases of the clotting reaction. These changes are associated with the development of pulmonary hypertension.

2. When dogs were given an active fibrinolysin followed by an infusion of whole amniotic fluid, the alterations in the clotting mechanism were either delayed or did not appear. No pulmonary hypertension developed in these animals.

3. We infer that infusions containing particulate matter will produce in dogs both pulmonary hypertension and changes in the clotting mechanism. Although these are independent changes, both are as closely related to the damage to the pulmonary vessels as they are to the biological nature of the infusions.

* Presented in part before the American Physiological Society [Federation Proc. 19: 56 (1960)].


 
  • References

  • (1) Rendelstein F. D. v, Frischauf H, Deutsch E. Über die gerinnungs-beschleunigende Wirkung des Fruchtwassers. Acta haemat. (Basel) 6: 18-31 1951;
  • (2) Schneider C L. Etiology of fibrinopenia: fibrination defibrination. Ann N Y Acad Sci. 75: 634-675 1959;
  • (3) Schneider C. L. Coagulation defects in obstetric shock; meconium embolism and heparin; fibrin embolism and defibrination. Amer. J. Obstet. Gynec. 69: 758-775 1955;
  • (4) Stefanini M, Turpini R. A. Fibrinogenopenie accident of pregnancy and delivery: a syndrome with multiple etiological mechanisms. Ann. N Y Acad Sei 75: 601-625 1959;
  • (5) Jaques W. E, Hampton J. W, Bird R. M, Bolten K. A, Randolph B. Pulmonary hypertension and plasma thromboplastin antecedent deficiency in dogs; experimental induction by infusion of amniotic fluid. A.M.A. Arch. Path. 69: 248-256 1960;
  • (6) Penick G. D, Roberts H. R, Webster W. P, Brinkhous K. M. Hemorrhagic states secondary to intravascular clotting. A.M.A. Arch. Path. 66: 708-714 1958;
  • (7) Kliman A, Alexander B, McKay D. Coagulation defect associated with the generalized Shwartzmann reaction. Fed. Proc. 18: 486 1959;
  • (8) Tocantins L. M. The coagulation of blood: methods of study. Grune and Stratton; New York: 1955
  • (9) Fowell A. H. Turbidimetric method of fibrinogen assay: results with the Coleman Junior spectrophotometer. Amer. J. clin. Path. 25: 340-342 1955;
  • (10) Biggs R, Macfarlane R. G. Human blood coagulation and its disorders. 2nd ed.. Charles C. Thomas; Ill. Springfield: 1957
  • (11) Johnson S. A, McClaughry R. I, Seegers W. H. Nature of the blood clotting mechanisms in hemophilia. J. Mich. med. Soc. 54: 797-800 1955;