Tissue Oxygen Utilization

1. Front Matter

   Pages i-ix

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2. Intracellular Oxygen Supply: Implications for Intensive Care

   • D. P. Jones, T. Y. Aw, D. P. Kowalski

   Pages 1-15

3. NMR Investigations of Cardiac Metabolism

   • A.-M. Seymour

   Pages 16-32

4. Evaluation of Tissue Hypoxia by Optical Methods

   • B. Chance

   Pages 33-40

5. Application of NIR Spectroscopy to Problems of Tissue Oxygenation

   • C. A. Piantadosi, W. J. Parsons, J. A. Griebel

   Pages 41-55

6. Principal Determinants of Tissue PO2: Clinical Considerations

   • T. E. Gayeski

   Pages 56-70

7. Cellular Metabolic Consequences of Altered Perfusion

   • H. Haljamäe

   Pages 71-86

8. Vascular Response to Hypoxia

   • J. Almirall, G. Hedenstierna

   Pages 87-102

9. Blood Rheology Factors and Capillary Blood Flow

   • K. Messmer

   Pages 103-113

10. Physiological and Pathological Oxygen Supply Dependency

    • S. M. Cain

    Pages 114-123

11. Oxygen Delivery and Utilization in Acute and Chronic Disease

    • D. R. Dantzker

    Pages 124-131

12. Oxygen Transport and Uptake in Health and Disease

    • P. T. Schumacker, R. W. Samsel

    Pages 132-142

13. Multiple Organ Oxygen Supply-Demand Relationships and Redistribution of Flow

    • R. Schlichtig, J. V. Snyder, M. R. Pinsky

    Pages 143-159

14. The Determinants of Maximum Oxygen Utilization: The Role of Hemoglobin Concentration

    • P. D. Wagner

    Pages 160-170

15. Oxygen Cost of Breathing

    • S. Zakynthinos, C. Roussos

    Pages 171-184

16. Myocardial Oxygen Metabolism in the Sepsis Syndrome

    • W. J. Sibbald

    Pages 185-199

17. Tissue Oxygen Utilization in Septic Shock

    • L. G. Thijs, A. B. J. Groeneveld

    Pages 200-216

18. Oxygen Supply Dependency in Septic Shock

    • J.-F. Dhainaut, G. Annat, A. Armaganidis

    Pages 217-226

19. Cellular Metabolism in Sepsis

    • G. Gutierrez, A. Dubin

    Pages 227-241

20. Multiple Organ Failure: Is It Only Hypoxia?

    • F. B. Cerra

    Pages 242-251

Disturbances in peripheral O extraction can be produced in dogs treated with 2 endotoxin and thereby provide an opportunity to test theories for the origin of pathological O supply dependency or to try different treatment modalities. The 2 most serious deficiency in the current animal models is the inability to mimic the increased O demand that is observed in patients at 02 delivery rates in excess of 2 normal. A particular feature of this increased O demand is that it apparently does 2 not stimulate increased 02 extraction, although the limitation in O extraction has 2 not been explored in patients by lowering 02 supply, for obvious reasons. At least two possibilities to account for increased 02 demand could be investigated in animal models, however. The amount of 02 that is utilized in extramitochondrial pathways, which is normally on the order of 10%, may be greatly increased in ARDS and sepsis by O radical formation. There is presently no information 2 concerning how much 02 might be used in this way. Another strong possibility is that mitochondrial injury, perhaps as a result of 02 radical formation, uncouples oxidative phosphorylation. Some evidence presently in the literature supports this idea [19]. Indeed, the association of increased blood lactate levels with higher than expected 02 demands makes uncoupling a very attractive hypothesis that warrants further investigation in animal models using such agents as 2,4-dinitrophenol. References 1.

• Hypoxie
• Intensivmedizin
• Sauerstoffzufuhr und -verbrauch
• Sepsis
• Surgery
• anesthesia
• care
• hypoxia
• intensive care
• intensive care medicine
• multiple organ failure
• oxygen delivery and consumption
• shock
• tissue
• zellulärer Stoffwechsel

• Pulmonary Medicine, Health Science Center, Houston, USA

  Guillermo Gutierrez

• Department of Intensive Care, Erasme University Hospital, Free University of Brussels, Brussels, Belgium

  Jean Louis Vincent

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