Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Oxygen supply dependency in the critically ill--a continuing conundrum.

S M Cain1

  • 1Department of Physiology and Biophysics, University of Alabama, Birmingham 35294-0005.

Advances in Experimental Medicine and Biology
|January 1, 1992
PubMed
Summary

Endotoxin in animal models mimics critical illness oxygen extraction defects. However, this study suggests endotoxin-induced issues may not always mean widespread tissue hypoxia, highlighting sepsis as a metabolic disease.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

A ventilatory effect of carbonic anhydrase inhibition in man.

Project report. USAF School of Aviation Medicine·2014
Same author

Respiratory effects of carbonic anhydrase inhibition.

Project report. USAF School of Aviation Medicine·2014
Same author

The conserved motif in hydrophilic loop 2/3 and loop 8/9 of the lactose permease of Escherichia coli. Analysis of suppressor mutations.

The Journal of membrane biology·2000
Same author

A structural change in the kinesin motor protein that drives motility.

Nature·2000
Same author

Myosin VI is an actin-based motor that moves backwards.

Nature·1999
Same author

Endothelial modulation of neural sympathetic vascular tone in canine skeletal muscle.

Journal of applied physiology (Bethesda, Md. : 1985)·1998

Area of Science:

  • Critical care medicine
  • Physiology
  • Pathophysiology

Background:

  • Endotoxin administration in animals replicates oxygen extraction defects seen in critically ill patients.
  • The central question is whether these defects signify pervasive tissue hypoxia or other metabolic disturbances.

Purpose of the Study:

  • To investigate if endotoxin-induced oxygen extraction defects in dogs necessarily indicate widespread tissue hypoxia.
  • To explore the role of endothelial damage and microvascular dysfunction in endotoxin-induced hypoxia.
  • To assess the reliability of arterial lactate levels in indicating tissue hypoxia during sepsis.

Main Methods:

  • Endotoxin treatment in experimental dogs to induce sepsis-like conditions.
  • Manipulation of arterial partial pressure of oxygen (PaO2) to assess oxygen diffusion limitations.

Related Experiment Videos

  • Administration of dichloroacetate (DCA) and dopexamine to evaluate metabolic and circulatory responses.
  • Regional lactate flux measurements to identify localized tissue hypoxia.

    • Main Results:

    • Altering PaO2 did not change critical oxygen delivery (DO2) or oxygen consumption (VO2) in endotoxic dogs, arguing against diffusion limitation.
    • Arterial lactate levels were not always indicative of widespread tissue hypoxia, as sepsis can cause lactacidosis via metabolic changes (e.g., pyruvate dehydrogenase inactivation) without hypoxia.
    • Regional lactate flux revealed gut hypoxia despite adequate DO2, attributed to blood flow maldistribution.

    Conclusions:

    • Endotoxin-induced oxygen extraction defects in experimental models may not equate to universal tissue hypoxia.
    • Sepsis is a complex metabolic disease where lactacidosis can occur independently of tissue oxygenation.
    • Further research using advanced noninvasive techniques is needed to accurately assess tissue oxygenation in critically ill patients with sepsis.