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Nitric oxide synthase activity in ulcerative colitis and Crohn's disease
N K Boughton-Smith1, S M Evans, C J Hawkey
1Wellcome Research Laboratories, Beckenham, Kent, UK.
Lancet (London, England)
|August 7, 1993
Summary
Elevated nitric oxide (NO) synthase activity in the colon mucosa is linked to ulcerative colitis, but not Crohn's disease. This finding suggests a role for NO in active ulcerative colitis inflammation and potential motility issues.
Area of Science:
- Gastroenterology
- Molecular Biology
- Immunology
Background:
- Inflammatory stimuli can induce nitric oxide (NO) synthase, leading to excessive NO production.
- Excessive NO contributes to vascular permeability changes and tissue injury.
- NO synthase activity in inflammatory bowel diseases is not fully understood.
Purpose of the Study:
- To measure and compare NO synthase activities in the colonic mucosa and muscle of patients with ulcerative colitis and Crohn's disease versus controls.
- To investigate the potential role of NO synthase induction in the pathophysiology of ulcerative colitis and Crohn's disease.
Main Methods:
- NO synthase activities were measured in colonic mucosal and muscle tissues.
- Samples were obtained from control patients, patients with ulcerative colitis, and patients with Crohn's disease.
- Statistical analysis was performed to compare enzyme activities between groups.
Main Results:
- NO synthase activity was approximately eightfold higher in the colonic mucosa of ulcerative colitis patients compared to controls (p < 0.001).
- No significant difference in NO synthase activity was observed in the colonic muscle of ulcerative colitis patients or in any tissue from Crohn's disease patients compared to controls.
- Mucosal NO synthase activity in Crohn's disease patients did not differ from control values.
Conclusions:
- The induction of colonic NO synthase in the mucosa is implicated in the mucosal vasodilation and increased vascular permeability characteristic of active ulcerative colitis.
- Elevated NO synthase activity may also contribute to the impaired motility observed in toxic dilation associated with ulcerative colitis.
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