Thrombolytic Agents: Biologic Properties and Issues Regarding Products Derived by Recombinant DNA Technology

  • Gene Murano
Part of the Developments in Cardiovascular Medicine book series (DICM, volume 100)

Abstract

Fibrin deposition plays a role not only in hemostasis, but also in the inflammatory response, defense mechanisms against bacterial invasion, and wound healing. For this mechanism that is perpetually ready to spring into action, the body pays the price of potential accumulation of fibrin microdeposits which constitute a hazard: thrombosis. Counterbalancing this potential danger is the fibrinolytic system which destroys fibrin deposits. In this respect, fibrin deposition may be considered a fundamental mechanism of injured tissue repair and fibrinolysis (thrombolysis) its physiologic antithesis.

Keywords

Fermentation Carbohydrate Mold Aspirin Heparin 

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General References

  1. 1.
    Bell WR. Thrombolytic therapy: a comparison between urokinase and streptokinase. Sem Thromb Hemost 1975; 2: 1–13.Google Scholar
  2. 2.
    Paoletti R, Sherry S (eds). Thrombosis and urokinase. Academic Press London, 1977; pp. 257.Google Scholar
  3. 3.
    Martin M. Streptokinase in chronic arterial disease, C.R.C. Press, Boca Raton, 1982; pp. 196.Google Scholar
  4. 4.
    Aoki N (volume ed). Fibrinolysis. Sem Thromb Hemost 1985; 10: 1–107.Google Scholar
  5. 5.
    Collen D, Lijnen HR, Verstraete M (eds). Thrombolysis. Biological and therapeutic properties of new thrombolytic agents. Churchill Livingstone, N.Y., 1985; pp. 173.Google Scholar
  6. 6.
    Bode C, Matsueda GH, Hui KY, Haber E. Antibody-directed urokinase: a specific fibrinolytic agent. Science 1985; 229: 765–767.PubMedCrossRefGoogle Scholar
  7. 7.
    Verstraete M, Collen D. Thrombolytic therapy in the eighties. Blood 1986; 67: 1529–1541.PubMedGoogle Scholar
  8. 8.
    Sobel BE, Collen D, Grossbard EB, (eds). Tissue plasminogen activator in thrombolytic therapy. Marcel Dekker, Inc. N.Y./Basel, 1987; pp. 241.Google Scholar
  9. 9.
    Samama MM. (volume ed). Thrombolytic agents and treatments. Sem Thromb Hemost 1987; 13: 131–242.CrossRefGoogle Scholar
  10. 10.
    Liu DT, Goldman H, Gates F. Consideration of the proteins and peptides produced by new technology for use as therapeutics. In: Delivery systems for peptide drugs. NATO ASI series A. Life Sciences 1987; 125: 341–349.Google Scholar
  11. 11.
    Gates FT. Regulating new technologies. Pharmaceutical Engineering 1987; 7: 22–25.Google Scholar
  12. 12.
    GISSI. Long term effects of intravenous thrombolysis in acute myocardial infarction: Final report of GISSI study. Lancet 1987; 2:871–874.Google Scholar
  13. 13.
    ISIS-2 (Second International Study of infarct survival) Collaborative Group. Randomized trial of intravenous streptokinase, oral aspirin, both, or neither among 1787 cases of suspected acute myocardial infarction: ISIS-2. Lancet 1988; 2:349–360.Google Scholar
  14. 14.
    AIMS Trial Study Group. Effect of intravenous APSAC on mortality after acute myocardial infarction: Preliminary report of a placebo-controlled clinical trial. Lancet 1988; 1:545–549.Google Scholar
  15. 15.
    ASSET Trial Study Group. Trial of Tissue plasminogen activator for mortality reduction in acute myocardial infarction. Lancet 1988; 2:525–530.Google Scholar
  16. 16.
    Collen D, Stassau JM, Larsen G. Pharmacokinetics and thrombolytic properties of deletion mutants of human tissue-type plasminogen activator in rabbits. Blood 1988; 71:216–219.PubMedGoogle Scholar
  17. 17.
    Marder YJ, Sherry S. Thrombolytic therapy: current status. N Engl J Med 1988; 318: 1512–1520 and 1585–1594.PubMedCrossRefGoogle Scholar

Copyright information

© Kluwer Academic Publishers 1989

Authors and Affiliations

  • Gene Murano
    • 1
  1. 1.Division of Blood and Blood ProductsCenter for Biologics Evaluation and ResearchBethesdaUSA

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