Oxidative stress and endothelial dysfunction during sepsis

Front Biosci (Landmark Ed). 2011 Jan 1;16:1986-95. doi: 10.2741/3835.

Abstract

Endothelial activation and dysfunction play a key role in the pathogenesis of sepsis. During septic shock, endothelial dysfunction is involved in microcirculation impairment and organ dysfunction. Reactive oxygen species (ROS) and reactive nitrogen species (RNS) have several potentially important effects on endothelial function and are implicated in physiological regulation and disease pathophysiology. The imbalance between the production of ROS and their effective removal by non-enzymatic and enzymatic antioxidants systems could induce endothelial dysfunction with alterations of vascular tone, increases in cell adhesion properties (leukocytes and platelet adhesion), increase in vascular wall permeability and a pro-coagulant state. Increasing evidence supports the idea that the principal cause of EC dysfunction during sepsis is cell injury. ROS and RNS contribute to mitochondrial dysfunction by a range of mechanisms and induce both necrotic and apoptotic cell death. Understanding the mechanisms underlying the generation of ROS and RNS in endothelial cells and the causes of endothelial dysfunction in sepsis may help provide therapeutic strategies to tackle endothelial dysfunction and microcirculatory failure in sepsis.

Publication types

  • Review

MeSH terms

  • Endothelium, Vascular / physiopathology*
  • Humans
  • Microcirculation / drug effects
  • Nitric Oxide Synthase Type II / metabolism
  • Oxidative Stress / physiology*
  • Reactive Nitrogen Species / metabolism
  • Reactive Oxygen Species / metabolism
  • Sepsis / physiopathology*
  • Shock, Septic / physiopathology

Substances

  • Reactive Nitrogen Species
  • Reactive Oxygen Species
  • Nitric Oxide Synthase Type II