Adequacy of gut oxygenation in endotoxemia and sepsis

To provide a succinct overview of current notions regarding sepsis-induced alterations in mesenteric perfusion and oxygen transport.

Selected English-language articles dealing with mesenteric perfusion and gut mucosal function during sepsis or endotoxicosis in experimental animals or man.

The review emphasizes findings obtained using a well-characterized porcine model of acute, resuscitated endotoxicosis. Other experimental and clinical studies are discussed as well.

Total hepatosplanchnic perfusion and oxygen uptake are increased in most patients with compensated sepsis. No data are currently available from clinical studies regarding the effect of sepsis on mesenteric perfusion per se. Data are unavailable regarding either total hepatosplanchnic or mesenteric blood flow in patients with decompensated sepsis (i.e., septic shock). Therefore, current ideas regarding mesenteric perfusion in sepsis derive primarily from studies using animal models. In a normodynamic porcine endotoxicosis model, mesenteric perfusion and oxygen delivery (DO2) are markedly decreased. The changes in flow and DO2 are accompanied by intestinal mucosal acidosis and increased permeability to hydrophilic solutes, suggesting that these latter phenomena are a consequence of lipopolysaccharide-induced mesenteric hypoperfusion. This idea is supported by the observation that maintenance of normal mesenteric blood flow ameliorates gut mucosal acidosis and hyperpermeability in endotoxic pigs. However, because transmesenteric oxygen consumption is unchanged in endotoxic pigs, the precise mechanistic relationship between hypoperfusion and altered barrier function remains puzzling.

Mesenteric hypoperfusion may be an important factor leading to alterations in gut epithelial permeability in endotoxicosis and sepsis.