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Redox imbalance in the critically ill.

J M Gutteridge1, J Mitchell

  • 1Oxygen Chemistry Laboratory, Royal Brompton and Harefield NHS Trust, London, UK.

British Medical Bulletin
|March 1, 2000
PubMed
Summary
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Sepsis and ARDS in critically ill patients cause vascular dysfunction through oxidative stress. Uncontrolled reactive oxygen and nitrogen species damage endothelium, leading to hypotension and pulmonary hypertension.

Area of Science:

  • Critical care medicine
  • Vascular biology
  • Oxidative stress research

Background:

  • Sepsis and ARDS are leading causes of death in intensive care.
  • These conditions involve disordered vascular control, including hypotension and pulmonary hypertension.
  • Patients with sepsis/SIRS and ARDS experience significant oxidative stress.

Purpose of the Study:

  • To investigate the role of oxidative stress in the vascular pathology of sepsis/SIRS and ARDS.
  • To understand the mechanisms by which reactive oxygen and nitrogen species contribute to endothelial injury.

Main Methods:

  • Review of experimental and clinical evidence.
  • Analysis of the uncontrolled production of reactive oxygen species (ROS) and reactive nitrogen species (RNS).

Related Experiment Videos

Main Results:

  • Uncontrolled ROS and RNS production initiates the vascular pathology in sepsis/SIRS and ARDS.
  • ROS and RNS modulate inflammatory cell adhesion.
  • ROS and RNS cause direct injury to the endothelium.

Conclusions:

  • Oxidative stress, driven by ROS and RNS, is a key factor in the vascular dysfunction seen in sepsis and ARDS.
  • Targeting ROS and RNS may offer therapeutic strategies for these critical conditions.