作者: Csaba Szabó , Andrew L. Salzman
DOI: 10.1007/978-3-0348-8960-5_12
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摘要: The free radical nitric oxide (NO) is generated by the five electron oxidation of a guanidino nitrogen from L-arginine group enzymes termed NO synthases (NOS). In past decade, it has become clear that this simple molecular species remarkable chemical versatility, allowing to participate in variety physiological and pathophysiological cellular processes lung [1]. been characterized, for example, as neurotransmitter [2], second messenger [3, 4], paracrine hormone [5, 6], cytotoxin 7]. Accordingly, production, distribution fate are tightly regulated [8–10]. Derangement balance may result state deficiency or excess [11], manifested inflammation [12–14], hypotension [15], transplant rejection [16], macromolecular epithelial hyperpermeability [17], hypertension [18], smooth muscle hyperplasia [19, 20] ischemia/reperfusion injury [21]. Currently, clinical investigations underway which level tissue pharmacologically manipulated exogenous delivery its gaseous form via inhibition synthases. proper application these approaches treatment pulmonary disease, well an understanding their anticipated side-effects, necessitates pathophysiologic role [3]. This review focuses on discusses potential therapeutic options management NO-related disease.