Complement and Shock

  • Desiree Armstrong
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 9)


Manifestations of shock are lowering of the blood pressure and pooling of blood in various vascular beds. Since the vascular system is permeated by the serum, any vasodilator or blood pressure-lowering agent which serum can make either per se, or because of foreign surfaces or injured tissues, might be formed in the vascular system. This is particularly true if the intrinsic potential of the serum for producing such a substance is very great, as it is for the plasma kinins (1, 2, 3, 4; for review articles, see 5, 6, 7, 8, and 9). “The very high kinin-forming potential of body fluids and tissues is in sharp contrast with the minute concentrations of kinins required for biological effects. One ml. of human plasma contains sufficient kininogenase and kininogen to produce in a few minutes kinin concentrations several thousand times higher than the levels effective on blood vessels. Full activation of this system in vivo would probably be lethal. A small fraction of the total potential is sufficient to produce any of the pathological changes attributed to kinins.” (10). These changes include vasodilatation and increase in capillary permeability; the large reserve capacity of this system is like those in various other biological systems such as the blood clotting system. Another system of the plasma capable of producing vasodilation, increase in capillary permeability and fall of blood pressure is the anaphylatoxin system, which seems to operate mainly by means of the histamine which it releases from the tissues (11, 12, 13, 14, 15, and 16) and by means of certain other blood pressure-lowering, shock-inducing agents and effects (17, 18, and 19). The kinin system also may operate through the action of intermediaries subsequent to the liberation of plasma kinin (20). It should not be forgotten that some of the various enzyme systems activated prior to the formation of the respective vasodilator, permeability-increasing end products may themselves also possess these properties.


Esterase Inhibitor Blood Clotting System Foreign Surface Kinin System Sodium Urate 
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  1. 1.
    Armstrong, D. and Stewart, J. W. (1960): Spontaneous plasma kinin formation in human plasma collected during labour. Nature (London), 188, 1193.CrossRefGoogle Scholar
  2. 2.
    Armstrong, D., Mills, G. L., and Sicuteri, F. (1966): Physiological influence on the liberation of human plasma kinin at low temperatures. Hypotensive Peptides, p. 139. Springer-Verlag, New York.CrossRefGoogle Scholar
  3. 3.
    Armstrong, D. (1969a): Hageman Factor and the spontaneous human plasma-kinin generation occurring in homogeneous media. Activation and inactivation. Inflammation, Biochemistry, and Drug Interaction, p. 153. Excerpta Medica Foundation, Amsterdam.Google Scholar
  4. 4.
    Armstrong, D. (1970a): Pain. Heffter’s Handbuch der Experimentellen Pharmakologie, Vol. 25. Springer-Verlag, Heidelberg. In press.Google Scholar
  5. 5.
    Lewis, G. P. (1960): Active polypeptides derived from plasma proteins. Physiological Reviews, 40, 647.PubMedGoogle Scholar
  6. 6.
    Lewis, G. P. (1962): Bradykinin — Biochemistry, Pharmacology and its physiological role in controlling local blood flow. Lectures on the Scientific Basis of Medicine, 14, 242.Google Scholar
  7. 7.
    Schachter, M. (1964): Kinins — a group of active peptides. Annual Reviews of Pharmacology, 4, 281.CrossRefGoogle Scholar
  8. 8.
    Erdos, E. G. (1966): Hypotensive peptides; bradykinin; kallidin and eledoisin. Advances in Pharmacology, 4, 1.PubMedCrossRefGoogle Scholar
  9. 9.
    Erdos, E. G. (1970): Bradykinin: kallidin: kallikrein. Heffter’s Handbuch der Experimentellen Pharmakologie, Vol. 25, Springer-Verlag, Heidelberg. In press.Google Scholar
  10. 10.
    Eisen, V. (1969): Kinin formation in human diseases. Lectures on the Scientific Basis of Medicine. Annual Review, p. 146. The Athlone Press, University of London, London.Google Scholar
  11. 11.
    Hahn, F. and Oberdorf, A. (1950): Antihistaminica und anaphylaktoide reaktionen. Zeitschrift für Immunologische-forschung, 107, 528.Google Scholar
  12. 12.
    Hahn, F., Lange, A., and Giertz, H. (1954): Anaphylaktoide reaktionen durch kunstliche blutersatzstoffe. Archiv für Experimentelle Pathologie und Pharmakologie, 222, 603.Google Scholar
  13. 13.
    Rocha e Silva, M., Bier, O., and Aronson, M. (1951): Histamine release by anaphylatoxin. Nature (London), 168, 465.CrossRefGoogle Scholar
  14. 14.
    Rocha e Silva, M. (1954): Anaphylatoxin and histamine release. Quarterly Reviews of Allergy, 8, 220.Google Scholar
  15. 15.
    Dias da Silva, W. and Lepow, I. H. (1965): Anaphylatoxin formation by purified human C’1 esterase. Journal of Immunology, 95, 1080.Google Scholar
  16. 16.
    Dias da Silva, W. and Lepow, I. H. (1967): Complement as a mediator of inflammation. II. Biological properties of anaphylatoxin prepared with purified components of human complement. Journal of Experimental Medicine, 125, 921.PubMedCrossRefGoogle Scholar
  17. 17.
    Friedberg, K. D., Engelhardt, G., and Meineke, F. (1965): Uber die tachyphylaxie der anaphylatoxinreaction und ihre bedeutung für die anaphylaxie. International Archives of Allergy and Applied Immunology, 25, 154.CrossRefGoogle Scholar
  18. 18.
    Hahn, F. (1967): Anaphylatoxin and anaphylaxis. Allergology, p. 145. Montreal.Google Scholar
  19. 19.
    Vogt, W. (1967): The anaphylatoxin-forming system. Reviews of Physiological Biochemistry and Experimental Pharmacology, 59, 160.Google Scholar
  20. 20.
    Piper, P. J. and Vane, J. R. (1969): Release of additional factors in anaphylaxis and its antagonism by antiinflammatory drugs. Nature (London), 223, 29.CrossRefGoogle Scholar
  21. 21.
    Friedberger, E. (1910): Weitere Untersuchungen uber eiweis-sanaphylaxie. IV. Mitteilung. Zeitschrift für Immunologischeforschung, 4, 636.Google Scholar
  22. 22.
    Smink, R. D., Jr., Abernethy, R. W., Ratnoff, O. D., and Lepow, I. H. (1964): Enhancement of vascular permeability by mixtures of C—1 esterase and normal serum. Proceedings of the Society for Experimental Biology and Medicine, 116, 280.PubMedGoogle Scholar
  23. 23.
    Cotran, R. S. and Majno, G. (1964): A light and electron microscopic analysis of vascular injury. Annals of the New York Academy of Science, 116, 750.CrossRefGoogle Scholar
  24. 24.
    Hahn, F. (1960): Anaphylatoxin: formation, actions and role in anaphylaxis. Polypeptides Which Affect Smooth Muscles and Blood Vessels. Pergamon Press, Oxford.Google Scholar
  25. 25.
    Budzko, D. B. and Muller-Eberhard, H. (1969): Anaphylatoxin release from the third component of human complement by hydroxylamine. Science, 165, 506.PubMedCrossRefGoogle Scholar
  26. 26.
    Rocha e Silva, M. and Carvalho, I. F. (1967): Anaphylatoxin and the kinin system. Allergology, p. 160. Pergamon Press, New York.Google Scholar
  27. 27.
    Armstrong, D., Jepson, J. B., Keele, C. A., and Stewart, J. W. (1957): Pain-producing substance in human inflammatory exudates and plasma. Journal of Physiology, 135, 350.PubMedGoogle Scholar
  28. 28.
    Movat, H. Z. (1967): Activation of the kinin system by antigen-antibody complexes. International Symposium on Vasoactive Polypeptides: Bradykinin and Related Kinins, p. 177, Edart Livraria Editora Ltda, Sao Paulo.Google Scholar
  29. 29.
    Margolis, J. (1960): The mode of action of Hageman Factor in the release of plasma kinin. Journal of Physiology, 151, 238.PubMedGoogle Scholar
  30. 30.
    Armstrong, D. and Mills, G. L. (1965): The reversible cold-induced activation of the plasma kinin-forming system between 37° and 0°C. Journal of Physiology, 179, 89.Google Scholar
  31. 31.
    Armstrong, D. (1969b): Actions of the human cold-activated plasma kinin-forming system of preheating at 56° and 60°C. Pharmacological Research Communications, 1, 30.CrossRefGoogle Scholar
  32. 32.
    Frey, E. K., Kraut, H., and Werle, E. (1950): Kallikrein (Padutin). Enke, Stuttgart.Google Scholar
  33. 33.
    Armstrong, D. (1968): The effects of temperature on the response of human plasma kinin-forming system to promoting and inhibiting agents. British Journal of Pharmacology, 34, 670P.Google Scholar
  34. 34.
    Donaldson, V. H. (1968): Mechanisms of activation of C’1 esterase in hereditary angioneurotic edema plasma in vitro. The role of Hageman Factor, a clot-promoting agent. Journal of Experimental Medicine, 127, 411.PubMedCrossRefGoogle Scholar
  35. 35.
    Pensky, J., Levy, L. E., and Lepow, I. H. (1961): Partial purification of a serum inhibitor of C’1 esterase. Journal of Biological Chemistry, 236, 1674.PubMedGoogle Scholar
  36. 36.
    Pensky, J. (1969): Personal communication.Google Scholar
  37. 37.
    Kellermeyer, R. W. and Breckenridge, R. T. (1965): The inflammatory process in acute gouty arthritis. I. Activation of Hageman Factor by sodium urate crystals. Journal of Laboratory and Clinical Medicine, 65, 307.PubMedGoogle Scholar
  38. 38.
    Eisen, V. (1966): Urates and kinin formation in synovial fluid. Proceedings of the Royal Society of Medicine, 59, 302.PubMedGoogle Scholar
  39. 39.
    Dias da Silva, W. and Armstrong, D. (1968): Unpublished observations.Google Scholar
  40. 40.
    Heidelberger, M. (1941): Quantitative chemical studies on complement of alexin. I. A Method. Journal of Experimental Medicine, 73, 681.PubMedCrossRefGoogle Scholar
  41. 41.
    Heidelberger, M., Rocha e Silva, M., and Mayer, M. M. (1941): Quantitative chemical studies on complement or alexin. III. Uptake of complement nitrogen under varying experimental conditions. Journal of Experimental Medicine, 74, 359.PubMedCrossRefGoogle Scholar
  42. 42.
    Naff, G. B., Pensky, J., and Lepow, I. H. (1964): The macro-molecular nature of the first component of human complement. Journal of Experimental Medicine, 119, 593.PubMedCrossRefGoogle Scholar
  43. 43.
    Cuschieri, A., Onabanjo, A. O., and James, P. B. (1969): Kinin release during cold vasodilatation. Pharmacological Research Communications. 1, 147.CrossRefGoogle Scholar
  44. 44.
    Kulka, J. P. (1964): Microcirculatory impairment as a factor in inflammatory tissue damage. Annals of the New York Academy of Science, 116, 1018.CrossRefGoogle Scholar
  45. 45.
    Armstrong, D., Mills, G. L., and Stewart, J. W. (1967): Thermally-induced effects on the kinin-forming system of native human plasma, 37°-0°C and 37°-50°C. International Symposium on Vasoactive Polypeptides: Bradykinin and Related Kinins, p. 167. Edart Livraria Editora Ltda, Sao Paulo.Google Scholar
  46. 46.
    Goodwin, L. G., Jones, C. R., Richards, W. H. G., and Kohn, J. (1963): Pharmacologically active substances in the urine of burned patients. British Journal of Experimental Pathology, 44, 551.PubMedGoogle Scholar

Copyright information

© Plenum Press, New York 1970

Authors and Affiliations

  • Desiree Armstrong
    • 1
  1. 1.Department of PharmacologyMiddlesex Hospital Medical SchoolLondon W. 1England

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