The pathogenesis of inflammatory disease: Surgical shock and multiple system organ failure

Chronic inflammatory disease, embracing rheumatoid arthritis (RA), inflammatory bowel disease (IBD), hepatitis, asthma, atherosclerosis, multiple system organ failure (MSOF), etc., is mediated by reactive oxygen species (ROS). These ROS originate from activated neutrophils in infections and in immune and autoimmune reactions, from tissue deposits of ferritin, and from futile cycling of cytochrome P450 (CYP) following exposure to persistent chemicals, and may be perpetuated by the actions of complement, cytokines and eicosanoids. Acute inflammation is normally arrested by removal of ROS by tissue glutathione (GSH) and the antioxidant vitamins, A, C and E, all of which are regenerated by NADH and NADPH. Failure of this antioxidant defence system can lead to oxidative stress and to chronic inflammatory disease, including surgical shock and MSOF. The roles of oxidative stress and microcirculatory arrest in promoting MSOF, and of GSH, the antioxidant defence system, and fibronectin in preventing this, are reviewed in the light of recent experimental studies of surgical shock, including fasting, anaesthesia, hepatic ischaemia and reperfusion.

• Publication year

  1995

• Venue

  InflammoPharmacology

• Publication date

  1995-06-01

• Fields of study

  Biology, Medicine

• Identifiers
  DOI 10.1007/BF02674919PMCID 7101736
• External record

  Open on Semantic Scholar

• Source metadata

  Semantic Scholar

• No claims are published for this paper.

• No concepts are published for this paper.

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