ABSTRACT
The potential causes of diminished smooth muscle contraction include inflammatory cells or inflammatory mediators. In both Crohn’s disease and ulcerative colitis, inflammatory cells infiltrate the mucosa. Colonic smooth muscle tension decreased slightly after exposure with the supernatants of unstimulated neutrophils and calcium ionophore-stimulated neutrophils when compared to incubation with Krebs solution alone. Arachidonic acid metabolites produced through the cyclooxygenase or lipoxygenase pathway are associated with mucosal inflammation, and possibly inhibit smooth muscle contraction. Rectal mucosa obtained from patients with active ulcerative colitis produces more prostaglandin E2 compared to healthy mucosa. Decreased smooth muscle force development associated with contiguous mucosal inflammation is not unique to the colon in ulcerative colitis. The lower esophageal sphincter is decreased when the mucosa is inflammed in reflux esophagitis. The absence of segmenting contractions of colonic muscle in ulcerative colitis can potentiate the secretory diarrhea of ulcerative colitis.
