BACKGROUND: Studies in animals indicate that inflammation causes changes in smooth muscle contractility. Because Crohn's disease is associated with altered motility, this study investigated the contractility of intestinal muscle resected from patients with or without Crohn's disease. METHODS: The isometric contraction of muscle strips from the small bowel of 36 patients with and 24 patients without Crohn's disease was examined. RESULTS: In longitudinal muscle from patients with Crohn's disease, there was a 55% increase in maximum contraction induced by carbachol but not histamine, but there was no change in the 50% effective dose (ED50) for these agonists. In contrast, in circular muscle from patients with Crohn's disease there was a sevenfold decrease in the ED50 value for carbachol but no change in maximum contraction. There was a 2.5-fold increase in the maximum response to histamine, but no change in ED50, in circular muscle from patients with Crohn's disease. However, there was no change in KCl-induced contraction between the two groups. The carbachol responses were atropine sensitive. Histamine responses were blocked by the H1 antagonist mepyramine but were not altered by a diamine oxidase inhibitor. All responses were tetrodotoxin insensitive. CONCLUSION: These results show altered receptor-mediated contraction in small intestinal muscle in patients with Crohn's disease.
BACKGROUND: Studies in animals indicate that inflammation causes changes in smooth muscle contractility. Because Crohn's disease is associated with altered motility, this study investigated the contractility of intestinal muscle resected from patients with or without Crohn's disease. METHODS: The isometric contraction of muscle strips from the small bowel of 36 patients with and 24 patients without Crohn's disease was examined. RESULTS: In longitudinal muscle from patients with Crohn's disease, there was a 55% increase in maximum contraction induced by carbachol but not histamine, but there was no change in the 50% effective dose (ED50) for these agonists. In contrast, in circular muscle from patients with Crohn's disease there was a sevenfold decrease in the ED50 value for carbachol but no change in maximum contraction. There was a 2.5-fold increase in the maximum response to histamine, but no change in ED50, in circular muscle from patients with Crohn's disease. However, there was no change in KCl-induced contraction between the two groups. The carbachol responses were atropine sensitive. Histamine responses were blocked by the H1 antagonist mepyramine but were not altered by a diamine oxidase inhibitor. All responses were tetrodotoxin insensitive. CONCLUSION: These results show altered receptor-mediated contraction in small intestinal muscle in patients with Crohn's disease.
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