Nitric oxide II. Nitric oxide protects in intestinal inflammation

This article examines the evidence for nitric oxide (NO) as a protective ag ent in splanchnic ischemia-reperfusion and other forms of acute intestinal inflammation. Four major paints emerge from this body of data. First, acute intestinal inflammation results in an early (i.e., <5 min) and severe decr ease in endothelium-derived NO. Thus the early trigger event in this condit ion is a functional loss of NO. Second, administration of exogenous NO, NO donors, or NO precursors ameliorate splanchnic ischemia-reperfusion and oth er forms of acute intestinal inflammation (i.e., splanchnic trauma). These beneficial effects occur at physiological levels of NO when given early in the course of the inflammatory state. Third, blockade of nitric oxide synth ase (NOS) or gene deletion of NOS exacerbates intestinal inflammation. Four th, there are a variety of signaling mechanisms that may mediate the protec tive effect of NO.