Advertisement

The Effect of Multiple Organ Failure on the Regulation of the Circulation with Special Reference to the Microcirculation

  • David H. Lewis

Abstract

The evolution of shock research in the latter half of this century has been one of investigating more and more complex experimental models as the mechanisms behind the less complex clinical situations become better understood. Such an understanding has usually led quite quickly to clinical application of the newly gained information. Thus, pure hemorrhagic shock models gave way to models of combined traumatic-hemorrhagic shock, and these have in turn given way to models of sepsis-endotoxin shock. It is also true that the clinical situations are never as “pure” as the experimental models, so that while trauma and sepsis can be separated in the laboratory they are often combined in the clinic. Failure to recover from these pathological conditions in a relatively rapid time frame leads to organ failure and at the end of the line is the specter multiple organ failure.

Keywords

Myocardial Blood Flow Multiple Organ Failure Postcapillary Venule Sympathoadrenal System Myocardial Blood Volume 
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.

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    Burnstock G, Griffith SG, Sneddon P (1984) Autonomic nerves in the precapillary vessel wall. J Cardiovasc Pharmacol 6: S344–S353PubMedCrossRefGoogle Scholar
  2. 2.
    Lundberg JM, Fried G, Pernow J, Theodorsson-Norheim E (1986) Corelease of neuropeptide Y and catecholamines upon adrenal activation in the cat. Acta Physiol Scand 126: 231–238PubMedCrossRefGoogle Scholar
  3. 3.
    McKechnie K, Dean HG, Furman BL, Parratt JR (1985) Plasma catecholamines during endotoxin infusion in conscious unrestrained rats: Effects of adrenal demedullation and/or guanethedine treatment Circ Shock 17: 85–94PubMedGoogle Scholar
  4. 4.
    Lewis DH (1987) Do the sympathetics play a role in the maintenance of microvascular hematocrit? Fed Proc 46: 1532Google Scholar
  5. 5.
    Lipowsky HH, Usami S, Chien S (1980) In vivo measurement of “apparent viscosity” and microvessel hematocrit in the mesentery of the cat Microvasc Res 19: 297–319PubMedCrossRefGoogle Scholar
  6. 6.
    Lewis DH, Schmid-Schönbein H (1981) Rheology and vasomotion: A validation of hemodilution as a rational therapeutic manuever. In: Schmid-Schönbein H, Messmer K, Rieger H (eds) Hemodilution and flow improvement. Bibliohca Haemat nr. 47. Karger, Basel, pp 122–126Google Scholar
  7. 7.
    Fukuyama T, Sobel BE, Roberts R (1984) Microvascular deterioration: implications for reperfusion. Cardiovasc Res 18: 310–320PubMedCrossRefGoogle Scholar
  8. 8.
    Engler RL, Schmid-Schönbein GV, Pavelec RS (1983) Leukocyte capillary plugging in myocardial ischemia and reperfusion in the dog. Am J Pathol 111: 96–111Google Scholar
  9. 9.
    Bond RF, Bond CH, Peissner LC, Manning ES (1981) Prostaglandin modulation of adrenergic vascular control during hemorrhagic shock. Am J Physiol 241: H85–H90PubMedGoogle Scholar
  10. 10.
    Jorfeldt L, Lewis DH, Löfström JB, Post C (1983) Lung uptake of lidocaine in man as influenced by anesthesia, mepivicaine infusion or lung insufficiency. Acta Anesthesiol Scand 27: 5–9CrossRefGoogle Scholar
  11. 11.
    Furchgott RF, Zawadski JV (1980) The obligatory role of endothelial cells in the relaxation of arterial smooth muscle by acetylcholine. Nature 288: 373–376PubMedCrossRefGoogle Scholar
  12. 12.
    Rosenblum WI, Nelson GH, Povlishock JT (1987) Laser-induced endothelial damage inhibits endothelium-dependent relaxation in the cerebral microcirculation of the mouse. Circ Res 60: 169–176PubMedGoogle Scholar
  13. 13.
    Shepherd JT, Vanhoutte PM (1985) Spasm of the coronary arteries: Causes and consequences (the scientists’ viewpoint). Mayo Clin Proc 60: 33–46PubMedGoogle Scholar
  14. 14.
    Lewis DH, Gidlöf A, Behm KE, Bengtsson M-B, Menschik A (1987) White cells in shock ischemia. In: Schlag G, Redl H (eds) First Vienna shock forum: A. Pathophysiological role of mediators and mediator inhibitors in shock. Liss, New York, pp 63–74Google Scholar
  15. 15.
    Gidlöf A, Lewis DH, Hammersen F (1988) The effect of prolonged total ischemia on the ultrastructure of human skeletal muscle capillaries. A morphometric analysis. Int J Microcirc: Clin Exp 7: 67–86Google Scholar

Copyright information

© Springer-Verlag Tokyo 1988

Authors and Affiliations

  • David H. Lewis
    • 1
  1. 1.Clinical Research Center, Faculty of Health SciencesUniversity HospitalLinköpingSweden

Personalised recommendations