Intracellular metabolite glutathione, existing in either its reduced (GSH) or oxidized states, is crucial for the protection of any cell against an oxidative stress or injury. Significant depletion of intracellular levels of GSH predisposes cells to an oxidative injury. We have investigated the level of hepatic GSH during the early course of sepsis in a physiologically well-characterized septic-sheep model. Following six hours of sepsis, which was characterized by hypotension, hypoxemia, and granulocytopenia, the level of intrahepatic GSH was significantly reduced compared with baseline levels. There was no reduction after two hours of sepsis. Hepatic GSH levels in control animals were unchanged compared with baseline levels. These findings suggest that the liver may be more susceptible to an oxidative stress in septic patients.
|Original language||English (US)|
|Number of pages||5|
|Journal||Archives of Surgery|
|State||Published - Aug 1985|