Suppression of lipopolysaccharide‐induced nitric oxide synthase expression by platelet‐activating factor receptor antagonists in the rat liver and cultured rat kupffer cells
Shamimunisa B. Mustafa, Brent D. Flickinger, Merle S. Olson – 30 December 2003 – Excessive nitric oxide (NO) generated by hepatic cells in response to lipopolysaccharide (LPS) and inflammatory substances (e.g., platelet‐activating factor [PAF]) is a key contributor to the pathophysiological outcomes observed in the liver during sepsis. In rats subjected to liver‐focused endotoxemia, inducible nitric oxide synthase (iNOS) levels in the intact liver were elevated by 6 hours; cell‐specific expression of iNOS messenger RNA (mRNA) was Kupffer cells (KCs), endothelial cells, and hepatocytes.