Manipulation of the L-arginine-nitric oxide pathway in experimental colitis

Br J Surg. 1995 Sep;82(9):1188-91. doi: 10.1002/bjs.1800820913.


The role of the L-arginine-nitric oxide pathway in the pathogenesis of colonic inflammation was assessed using L-arginine and its competitive analogue N omega-nitro-L-arginine methyl ester (L-NAME) in a rat model of colitis. In the first study oral L-arginine 2 per cent (control: 3.4 per cent L-glycine) was administered with and without L-NAME 100 mg/l. Orally administered L-arginine increased colonic inflammation (P = 0.004) and decreased thymic weight (P = 0.0007). Addition of L-NAME reduced the colonic inflammation and prevented loss of body-weight (P < 0.04). In the second study L-NAME was administered orally in concentrations of 100, 200 and 500 mg/l (control: no L-NAME). L-NAME 500 mg/l reduced colonic inflammation and increased thymic weight and body-weight (P < 0.01). Thymic weight and body-weight correlated positively with the concentration of L-NAME administered orally (rs > or = 0.3, P = 0.04). L-NAME l g/l was administered topically as an enema (control: suspension agent). Topical L-NAME reduced colonic inflammation and increased thymic weight (P < 0.05). These results suggest that the L-arginine-nitric oxide pathway mediates colonic inflammation in this model.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Administration, Oral
  • Administration, Topical
  • Animals
  • Arginine / analogs & derivatives*
  • Arginine / antagonists & inhibitors*
  • Arginine / pharmacology
  • Colitis / chemically induced
  • Colitis / metabolism*
  • Colon / drug effects*
  • Colon / pathology
  • Female
  • NG-Nitroarginine Methyl Ester
  • Nitric Oxide / antagonists & inhibitors*
  • Organ Size
  • Rats
  • Rats, Wistar
  • Trinitrobenzenesulfonic Acid / pharmacology*


  • Nitric Oxide
  • Trinitrobenzenesulfonic Acid
  • Arginine
  • NG-Nitroarginine Methyl Ester