Gastrointestinal mucosal injury in experimental models of shock, trauma, and sepsis

The mucosa of the GI tract serves as an important barrier limiting the systemic absorption of luminal microbes and microbial products. Two methods commonly used to assess the integrity of the GI mucosal barrier are assessment of the extent of microbial translocation and measurement of mucosal permeability to hydrophilic probes.

Studies using these methods have provided convincing evidence that the barrier function of the intestinal mucosa is deranged in numerous animal models of shock, trauma, and sepsis.

Although the mechanisms underlying mucosal injury under these circumstances remain incompletely understood, current evidence suggests that mucosal damage in shock, trauma, and sepsis is likely due to various combinations of intracellular hypoxia due to ischemia, tissue injury caused by reactive oxygen metabolites, the deleterious effects of various lipid mediators (e.g., platelet-activating factor) and/or cytokines (e.g., tumor necrosis factor), and deficient utilization or supply of key nutritional substrates (e.g., glutamine).