Pathophysiologic Mechanisms in Endotoxin Shock and its Therapeutic Approaches

  • H. Neuhof
  • E. Glaser
  • D. Hey
  • H. G. Lasch
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 9)


In comparative shock studies, one of the main problems is to find a parameter suitable for measuring the extent of organ damage during shock. Measuring the arterial, central venous and right ventricular pressure only yields very unreliable parameters, as f.i. even with an extremely diminished cardiac output, the arterial blood pressure may, as a compensatory mechanism, be raised above normal. The characteristic common to all forms of shock, regardless of their causative factor, is the acute insufficient blood flow in the circulation periphery. The limiting factor in shock is the insufficient oxygen supply of organs, which results in anaerobic metabolism with all its well-known metabolic consequences (1, 2). The continuous registration of the cardiac output, however, is rather intricate, and up to know has been mainly used in animal experiments. Besides, measuring the cardiac output without simultaneously measuring arterial and central venous blood gases, would not permit a quantitative conclusion as to the oxygen supply of the circulation periphery.


Oxygen Uptake Arterial Blood Pressure Pulmonary Circulation Platelet Aggregate Fibrinolytic Therapy 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.


Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.


  1. 1.
    Isselhard, W.: DMW 8: 349 (1965).CrossRefGoogle Scholar
  2. 2.
    Bing, R.J.: Fed. Proc. 19(9): 72 (1961).Google Scholar
  3. 3.
    Guyton, A.C. and J.W. Crowell: Fed Proc. 20(9): 51 (1961).PubMedGoogle Scholar
  4. 4.
    Crowell, J.W. and E.E. Smith: Am. J. Physiol. 206(2): 313 (1964).PubMedGoogle Scholar
  5. 5.
    Lasch, H.G.: Med.Welt 31: 1780 (1967).PubMedGoogle Scholar
  6. 6.
    Müller-Berghaus, G. und H.G. Lasch: Thrombos. Diathes. haemorrh. 9: 335 (1963).Google Scholar
  7. 7.
    McKay, D.G.: Disseminated Intravascular Coagulation (New York 1965).Google Scholar
  8. 8.
    Hardaway, R.M., E.A. Husni, E.F. Geever, H.E. Noyes and J.W. Burns: Ann.Surg. 154: 791 (1961).PubMedCrossRefGoogle Scholar
  9. 9.
    Robb, H.J.: Angiology 16: 405 (1965).CrossRefGoogle Scholar
  10. 10.
    Neuhof, H. und G. Kaufmann: Verh. Deutsch. Ges. Kreislaufforsch. 34: 218 (1968).PubMedGoogle Scholar
  11. 11.
    Hinshaw, L.B., J.A. Vick, C.H. Carlson and Y.L. Fan: Proc.Soc.exp.Biol. 104: 379 (1960).PubMedGoogle Scholar
  12. 12.
    Hinshaw, L.B., M.M. Jordan and J.A. Vick: J.Clin.Invest. 40: 1631 (1961).PubMedCrossRefGoogle Scholar
  13. 13.
    Hinshaw, L.B., R.E. Emerson, P.P. Iampietro and C.M. Brake: Am.J.Physiol, 203: 600 (1962).PubMedGoogle Scholar
  14. 14.
    Lee, L.: Z.exp.Med. 115: 1065 (1962).CrossRefGoogle Scholar
  15. 15.
    Sandritter, W. und H.G. Lasch: Meth.Achievm.exp.Path. 3: 86 (1967).Google Scholar
  16. 16.
    Kuhn, W. und H. Graeff: Septischer Abort und bakterieller Schock. Springer-Verlag, Berlin (1968).Google Scholar
  17. 17.
    Crowell, J.W. and W.L. Read: Am.J.Physiol. 183: 565 (1955).PubMedGoogle Scholar
  18. 18.
    Lasch, H.G. und H. Neuhof: Therapeutische und experimentelle Fibrinolyse. F.K.Schattauer-Verlag, Stuttgart (1969).Google Scholar

Copyright information

© Plenum Press, New York 1970

Authors and Affiliations

  • H. Neuhof
    • 1
  • E. Glaser
    • 1
  • D. Hey
    • 1
  • H. G. Lasch
    • 1
  1. 1.Department of Internal MedicineJustus Liebig-UniversityGiessenGermany

Personalised recommendations