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Rapid and persistent decrease in brain tissue oxygenation in ovine gram-negative sepsis.

Nobuki Okazaki1,2, Yugeesh R Lankadeva1, Rachel M Peiris1

  • 1Preclinical Critical Care Unit, Florey Institute of Neuroscience and Mental Health, University of Melbourne, Melbourne, Victoria, Australia.

American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
|November 17, 2021
PubMed
Summary
This summary is machine-generated.

Critical illness can impair brain function due to unclear changes in blood flow and oxygen. This study shows sepsis significantly reduces brain oxygen levels in sheep, potentially causing lethargy.

Keywords:
acute kidney injurycerebral oxygenationcerebral perfusionhypoxiasepsis

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Area of Science:

  • Physiology
  • Critical Care Medicine
  • Neuroscience

Background:

  • Brain dysfunction in critical illness is poorly understood due to measurement limitations.
  • Cerebral perfusion and oxygenation changes are implicated in critical illness-related brain dysfunction.
  • Lack of reliable methods hinders the study of brain variables during critical illness.

Purpose of the Study:

  • To develop and utilize a novel technique for chronic measurement of cerebral perfusion and oxygen tension in unanesthetized animals.
  • To investigate the dynamic changes in cerebral perfusion and oxygen partial pressure (Po2) during the development of ovine sepsis.
  • To correlate physiological changes during sepsis with alterations in brain oxygenation.

Main Methods:

  • Developed a chronic measurement technique using fiber-optic probes in unanesthetized sheep.
  • Implanted probes in brain, renal cortex, and medulla to measure tissue perfusion, Po2, and temperature.
  • Induced hyperdynamic sepsis by infusing live Escherichia coli for 24 hours, monitoring hemodynamic and tissue variables.

Main Results:

  • Sepsis induced hyperdynamic circulation with decreased mean arterial pressure and increased cardiac output.
  • A significant and sustained decrease in cerebral tissue Po2 was observed within 3 hours of sepsis onset.
  • Renal medullary perfusion and Po2 were significantly reduced, while the renal cortex remained unaffected.

Conclusions:

  • Ovine sepsis leads to an early and persistent decrease in cerebral Po2, independent of significant changes in cerebral perfusion.
  • Cerebral hypoxia is a likely contributor to sepsis-induced malaise and lethargy.
  • The developed technique enables chronic monitoring of brain variables in vivo during critical illness.