Abstract
The pathogenesis of non-steroidal anti-inflammatory drug (NSAID)-induced gastroenteropathy may involve a number of key events leading to increased intestinal permeability and inflammation (topical effect) and the development of ulcers (micro-vascular effects of COX-1 inhibition and prostaglandin deficiency). Many strategies have been employed in an attempt to reduce the toxic effects of NSAIDs and these have been targeted at the different pathogenic stages of lesion development. One of the latest in this long chain of damage limitation has been the development of nitric oxide (NO) sequestering NSAIDs (NO-NSAIDs). It is suggested that the NO, which is released as the compounds are broken down, may counteract the consequences of the NSAID-induced decrease in mucosal prostaglandins. Here we examine the proposed mechanisms for NSAID-induced gastrointestinal damage together with some of the methods employed to address these mechanisms. We also consider the physiologic roles of NO in the gut together with how it may be potentially employed as an agent for limiting the side effects of NSAIDs in the gastrointestinal tract.
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