Pathophysiology of Intestinal Inflammation in IBD: | Open Access
Matthew B Grisham, Satoshi Aiko, "Nitric oxide and chronic colitis", Canadian Journal of Gastroenterology and Hepatology, vol. 10, Article ID 673681, 4 pages, 1996. https://doi.org/10.1155/1996/673681
Nitric oxide and chronic colitis
Nitric oxide (NO) is thought to play an important role in modulating the inflammatory response by virtue of its ability to affect bloodflow, leukocyte function and cell viability. The objective of this study was to assess the role that NO may play in mediating the mucosal injury and inflammation in a model of chronic granulomatous colitis using two pharmacologically different inhibitors of nitric oxide synthase (NOS). Chronic granulomatous colitis with liver and spleen inflammation was induced in female Lewis rats via the subserosal (intramural) injection of peptidoglycan/polysaccharide (PG/PS) derived from group A streptococci. Chronic NOS inhibition by oral administration of NG-nitro-L-arginine methyl ester (L-NAME) (15 µmol/kg/day) or amino-guanidine (AG) (15 µmol/ kg/day) was found to attenuate the PG/PS-induced increases in macroscopic colonic inflammation scores and colonic myeloperoxidase activity. Only AG -- not L-NAME – attenuated the PG/PS-induced increases in colon dry weight. Both L-NAME and AG significantly attenuated the PG/PS-induced increases in spleen weight whereas neither was effective at significantly attenuating the PG/PS-induced increases in liver weight. Although both L-NAME and AG inhibited NO production in vivo, as measured by decreases in plasma nitrite and nitrate levels, only AG produced significantly lower values (38±3 versus 83±8 µM, respectively, P<0.05). Finally, L-NAME, but not AG, administration significantly increased mean arterial pressure from 83 mmHg in colitic animals to 105 mmHg in the PG/PS+ L-NAME-treated animals (P<0.05). It is concluded that NO may play an important role in mediating some of the pathophysiology associated with this model of chronic granulomatous colitis.
Copyright © 1996 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.