Fry D E, Kaelin C R, Giammara B L, Rink R D
Adv Shock Res. 1981;6:45-54.
To examine the mechanisms underlying organ failure and disordered cellular metabolism in sepsis, systemic oxygenation, hepatic tissue oxygenation, and hepatic mitochondrial metabolism were studied in rats subjected to an LD100 dose of E. coli bacteria administered intravascularly. The animals maintained normal systemic oxygenation and remained normotensive during the six-hour study period. Hepatic tissue pO2 declined nearly 90% in comparison to controls. Isolated hepatic mitochondria demonstrated statistically increased respiratory control indices that are characteristic of cellular hypoxia. Histologic examination of liver tissue showed obliteration of the sinusoids with debris and cellular aggregates. The data suggest that altered cellular oxygen delivery secondary to sinusoidal obliteration may have significance in hepatic failure and subsequent death in septic patients.
