Gut Oxygenation after Reduced Oxygen Delivery

Statements such as “the gut is the engine of sepsis” and the “gut is the canary of the body” are bandied about readily in the literature and in meetings of critical care specialists. The rationale for such statements is at least partially attributable to the fact that, in addition to its primary function to digest and to absorb nutrients, the gut also serves as a barrier to aid in the prevention of systemic contamination by microbes and microbial products [1]. If that barrier function is rendered incompetent for any reason, then the gut itself may contribute to multisystem organ failure, a frequent outcome in human sepsis. Integrity of the barrier function is undoubtedly threatened by the fact that the gut and the gut mucosal layer, in particular, appear to be extremely susceptible to hypoxic injury incurred during septic states. In that a reduction in oxygen delivery (DO2) is often a prominent feature of natural and experimental septic states, it would be useful to see whether reductions in DO2 by other means such as hemorrhagic shock and isovolemic hemodilution have similar effects on gut oxygenation. The main premise will be that the gut cannot be regarded as a single tissue with respect to its oxygenation. Indeed, the dichotomous behavior of the mucosal layer as opposed to the remainder of the gut wall must be considered for all aspects of its physiology and pathophysiology. At least some of the underlying reasons for this lie within its vascular architecture.