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Am J Physiol Gastrointest Liver Physiol 276: G572-G575, 1999;
0193-1857/99 $5.00
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Vol. 276, Issue 3, G572-G575, March 1999

THEMES
Nitric Oxide
II. Nitric oxide protects in intestinal inflammation*

Allan M. Lefer and David J. Lefer

Department of Physiology, Jefferson Medical College, Thomas Jefferson University, Philadelphia, Pennsylvania 19107; and Department of Physiology, Louisiana State University Medical Center, Shreveport, Louisiana 71130

This article examines the evidence for nitric oxide (NO) as a protective agent in splanchnic ischemia-reperfusion and other forms of acute intestinal inflammation. Four major points emerge from this body of data. First, acute intestinal inflammation results in an early (i.e., <5 min) and severe decrease in endothelium-derived NO. Thus the early trigger event in this condition is a functional loss of NO. Second, administration of exogenous NO, NO donors, or NO precursors ameliorate splanchnic ischemia-reperfusion and other 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 synthase (NOS) or gene deletion of NOS exacerbates intestinal inflammation. Fourth, there are a variety of signaling mechanisms that may mediate the protective effect of NO.

synthase blockers; nitric oxide donors; nitric oxide synthase gene-targeted mice; L-arginine


* Second in a series of invited articles on Nitric Oxide.




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