{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T10:57:21Z","timestamp":1789988241351,"version":"4.0.1"},"reference-count":31,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Gastrointestinal and Liver Physiology"],"published-print":{"date-parts":[[2001,2,1]]},"abstract":"<jats:p>In vitro, nitric oxide (NO) decreases leukocyte adhesion to endothelium by attenuating endothelial adhesion molecule expression. In vivo, lipopolysaccharide-induced leukocyte rolling and adhesion was greater in inducible NO synthase (iNOS)\u2212\/\u2212 mice than in wild-type mice. The objective of this study was to assess E- and P-selectin expression in the microvasculature of iNOS\u2212\/\u2212 and wild-type mice subjected to acute peritonitis by cecal ligation and perforation (CLP). E- and P-selectin expression were increased in various organs within the peritoneum of wild-type animals after CLP. This CLP-induced upregulation of E- and P-selectin was substantially reduced in iNOS\u2212\/\u2212 mice. Tissue myeloperoxidase (MPO) activity was increased to a greater extent in the gut of wild-type than in iNOS\u2212\/\u2212 mice subjected to CLP. In the lung, the reduced expression of E-selectin in iNOS\u2212\/\u2212 mice was not associated with a decrease in MPO. Our findings indicate that NO derived from iNOS plays an important role in sepsis-induced increase in selectin expression in the systemic and pulmonary circulation. However, in iNOS\u2212\/\u2212 mice, sepsis-induced leukocyte accumulation is affected in the gut but not in the lungs.<\/jats:p>","DOI":"10.1152\/ajpgi.2001.280.2.g291","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T15:43:42Z","timestamp":1514130222000},"page":"G291-G297","source":"Crossref","is-referenced-by-count":23,"title":["Endothelial E- and P-selectin expression in iNOS- deficient mice exposed to polymicrobial sepsis"],"prefix":"10.1152","volume":"280","author":[{"given":"Cameron W.","family":"Lush","sequence":"first","affiliation":[{"name":"Department of Physiology, University of Western Ontario, London, N6A 5C1; and Vascular Biology Program, Lawson Health Research Institute, London, Ontario, Canada, N6A 4G5"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gediminas","family":"Cepinskas","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Western Ontario, London, N6A 5C1; and Vascular Biology Program, Lawson Health Research Institute, London, Ontario, Canada, N6A 4G5"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William J.","family":"Sibbald","sequence":"additional","affiliation":[{"name":"Department of Physiology, University of Western Ontario, London, N6A 5C1; 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