Mucosal protection from intestinal ischemia-reperfusion reduces oxidant injury to the lung

J Surg Res. 1997 Nov;73(1):41-6. doi: 10.1006/jsre.1997.5196.


The authors investigated whether amelioration of intestinal mucosal injury, due to ischemia-reperfusion (I/R), with oxygenated perfluorocarbon (PFC) would reduce an oxidant-generated lung injury. The small intestine is increasingly recognized as a primary effector of distant organ injury. Clinical and experimental studies suggest oxidant species and activated neutrophils as the agents responsible for lung injury after intestinal I/R. The role of intestinal mucosal injury has not been defined. Oxygenated PFC was perfused through the lumen of the intestine during periods of I/R. Portal venous effluent was examined for reactive oxygen species and lung tissue was examined for lipid peroxidation. Luminal perfusion of oxygenated PFC during intestinal I/R reduced oxidant species in the portal blood. This correlated with a reduction in lung lipid peroxidation. Oxygenated PFC prevented intestinal mucosal injury resulting from induced I/R. Amelioration of mucosal injury reduced oxidant generation in the portal venous circulation that was proportional to the reduction in measured lung injury. Protection of the mucosa with intraluminal oxygen may prevent I/R-associated lung injury.

MeSH terms

  • Animals
  • Fluorocarbons
  • Intestinal Mucosa / pathology*
  • Intestines / blood supply*
  • Ischemia*
  • Lipid Peroxidation
  • Lung / metabolism
  • Lung Diseases / etiology
  • Lung Diseases / prevention & control
  • Male
  • Oxidants* / blood
  • Portal Vein
  • Rats
  • Rats, Sprague-Dawley
  • Reactive Oxygen Species / metabolism
  • Reperfusion Injury / chemically induced*
  • Reperfusion Injury / prevention & control*


  • Fluorocarbons
  • Oxidants
  • Reactive Oxygen Species