Nitric oxide synthase activity in ulcerative colitis and Crohn's disease

Excessive nitric oxide (NO) production by an isoform of NO synthase than can be induced by inflammatory stimuli leads to changes in vascular permeability and to tissue injury. We measured NO synthase activities in mucosa and muscle from the colons of control patients (n=11) and patients with ulcerat...

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Published inThe Lancet (British edition) Vol. 342; no. 8867; pp. 338,e1,e2 - 340,e1,e2
Main Authors Boughton-Smith, N.K., Evans, S.M., Whittle, B.J.R., Moncada, S., Hawkey, C.J., Cole, A.T., Balsitis, M.
Format Journal Article
LanguageEnglish
Published London Elsevier Ltd 07.08.1993
Lancet
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Summary:Excessive nitric oxide (NO) production by an isoform of NO synthase than can be induced by inflammatory stimuli leads to changes in vascular permeability and to tissue injury. We measured NO synthase activities in mucosa and muscle from the colons of control patients (n=11) and patients with ulcerative colitis (6) or Crohn's disease (4). NO synthase activity in colonic mucosa of ulcerative colitis patients was 0·55 (median interquartile range 0·32–0·57) nmol/min per g tissue, which was about eightfold higher than the value in control mucosa, with no individual overlap (p<0·001). With colonic muscle there was no difference in NO synthase activity between ulcerative colitis patients and controls. In the patients with Crohn's disease, mucosal NO synthase activity did not differ from control values and activity in the colonic muscle was low. Thus, induction of colonic NO synthase may be involved in the mucosal vasodilation and increased vascular permeability of active ulcerative colitis, and could also contribute to the impaired motility that accompanies toxic dilation. Lancet 1993; 342: 338–40
ISSN:0140-6736
1474-547X
DOI:10.1016/0140-6736(93)91476-3