| pubmed-article:7717775 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:7717775 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
| pubmed-article:7717775 | lifeskim:mentions | umls-concept:C0028128 | lld:lifeskim |
| pubmed-article:7717775 | pubmed:issue | 3 | lld:pubmed |
| pubmed-article:7717775 | pubmed:dateCreated | 1995-5-12 | lld:pubmed |
| pubmed-article:7717775 | pubmed:abstractText | Nitric oxide (NO) is a highly reactive free radical with a multitude of organ specific regulatory functions. Since 1985, NO has been the subject of numerous research efforts and as a result, has been found to play a major role in the cardiovascular, pulmonary, gastrointestinal, immune, and central nervous systems. In addition, deranged NO synthesis is the basis for a number of pathophysiologic states, such as atherosclerosis, pulmonary hypertension, pyloric stenosis, and the hypertension associated with renal failure. Traditional NO donors such as sodium nitroprusside and new pharmacologic NO adducts such as S-nitrosothiols may serve as exogenous sources of NO for the treatment of NO-deficient pathologic states. This review is an attempt to acquaint the surgical community with the fundamentals of NO biochemistry and physiology. Increased knowledge of its functions in normal homeostasis and pathologic states will enable physicians to better understand these disease processes and utilize new pharmacologic therapies. | lld:pubmed |
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