Critical O2 Delivery in Rat Brain

  • Robert Schlichtig
  • Jill Herrick
  • Edwin M. Nemoto
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 345)

Abstract

As O2 delivery (DO2) of whole body,1,2 intestine,3,4 liver,5 or skeletal muscle6 is progressively decreased in anesthetized animals, O2 consumption (VO2) is initially maintained constant via increased O2 extraction by the tissues (O2 supply independence). However, below a critical threshold DO2 value (DO2c), VO2 of these organs decreases in proportion to DO2 (O2 supply dependence). More importantly, dysoxia (i.e. O2 demand that exceeds O2 supply)7 appears to commence at the onset of liver O2 supply dependence, as reflected by the simultaneous decrease in VO2 and increase in hepatic mitochondrial reduction.5 Accordingly, it tentatively appears that dysoxia may be identified, in liver at least, by the DO2c inflection of a biphasic VO2- DO2 relation.

Keywords

Catheter Filtration Platinum Immobilization 

Preview

Unable to display preview. Download preview PDF.

Unable to display preview. Download preview PDF.

References

  1. 1.
    S.M. Cain. Peripheral oxygen uptake and delivery in health and disease. Clin. Chest Med. 4: 139–148 (1983).Google Scholar
  2. 2.
    S.A. Bowles, R. Schlichtig, H.A. Klions, D.J. Kramer. Arteriovenous pH and PCO2 detects critical O2 delivery during progressive hemorrhage in dogs. Journal of Critical Care 7: 95–105 (1992).CrossRefGoogle Scholar
  3. 3.
    D.P. Nelson, C.E. King, S.L. Dodd, P.T. Schumacker, S.M. Cain. Systemic and intestinal limits of O2 extraction in the dog. J. Appl. Physiol. 63: 387–394, 1987.PubMedGoogle Scholar
  4. 4.
    R. Schlichtig, D.J. Kramer, M.R. Pinsky. Flow redistribution during progressive hemorrhage is a determinant of critical O2 delivery. J. Appl. Physiol. 70: 169–178 (1991).PubMedGoogle Scholar
  5. 5.
    R. Schlichtig, H.A. Klions, D.J. Kramer, E.M. Nemoto. Hepatic dysoxia commences during O2 supply dependence. J. Appl. Physiol. 72: 1499–1505 (1992).PubMedGoogle Scholar
  6. 6.
    D.L. Bredle, R.W. Samsel, P.T. Schumacker, S.M. Cain. Critical O2 delivery to skeletal muscle at high and low PO2 in endotoxemic dogs. J. Appl. Physiol. 66: 2553–2558 (1989).PubMedGoogle Scholar
  7. 7.
    R.J. Connett, C.R. Honig, T.E.J. Gayeski, G.A. Brooks. Defining hypoxia: a systems view of VO2. glycolysis, energetics, and intracellular PO2. J. Appl. Physiol. 68: 833–842 (1990).PubMedGoogle Scholar
  8. 8.
    R. Schlichtig, D.J. Kramer, J. R. Boston, M.R. Pinsky. Renal O2 consumption during progressive hemorrhage. J. Appl. Physiol. 70: 1957–1962 (1991).PubMedCrossRefGoogle Scholar
  9. 9.
    C. Carlsson, M. Hagerdal, A.E. Kaasik, B.K. Siesjo. A catecholamine-mediated increase in cerebral oxygen uptake during immobilization stress in rats. Brain Res. 119: 223–231 (1977).PubMedCrossRefGoogle Scholar

Copyright information

© Springer Science+Business Media New York 1994

Authors and Affiliations

  • Robert Schlichtig
    • 1
    • 2
  • Jill Herrick
    • 2
  • Edwin M. Nemoto
    • 1
  1. 1.Department of Anesthesiology and Critical Care MedicineUniversity of PittsburghPittsburghUSA
  2. 2.Veterans Affairs Medical CenterUniversity DrivePittsburghUSA

Personalised recommendations