Abnormal contractile properties of rectal smooth muscle in chronic ulcerative colitis

Citation
Ta. Cook et al., Abnormal contractile properties of rectal smooth muscle in chronic ulcerative colitis, ALIM PHARM, 14(10), 2000, pp. 1287-1294
Citations number
28
Categorie Soggetti
Pharmacology,"da verificare
Journal title
ALIMENTARY PHARMACOLOGY & THERAPEUTICS
ISSN journal
02692813 → ACNP
Volume
14
Issue
10
Year of publication
2000
Pages
1287 - 1294
Database
ISI
SICI code
0269-2813(200010)14:10<1287:ACPORS>2.0.ZU;2-#
Abstract
Background: Patients with ulcerative colitis have abnormal rectal motility. Aim: To compare the contractile properties of rectal smooth muscle from pat ients with ulcerative colitis and controls. Methods: Rectal smooth muscle strips from patients undergoing resection for ulcerative colitis or cancer (control) were mounted in an organ bath. The effects of carbachol (receptor-mediated) and potassium (causes membrane dep olarization) were studied. Acetylcholinesterase histochemistry was performe d and nerve counts compared. Results: Ulcerative colitis (n=41) and control (n=34) strips contracted in response to potassium and carbachol. Mean (S.E.M.) maximum response to pota ssium in the control and ulcerative colitis groups was 1.07 (0.06) g/mg and 1.02 (0.09) g/mg tissue, respectively (P=N.S.). EC50s (concentrations requ ired to give 50% of maximal response) were 75 (1) mM and 73 (1) mM, respect ively (P=N.S.). Although maximum responses to carbachol were similar, 2.12 (0.12) g/mg and 1.95 (0.12) g/mg tissue (P=N.S.), ulcerative colitis strips exhibited an increased sensitivity to carbachol, EC50s: 5.05 x 10(-6) (0.5 5 x 10(-6)) M vs. 8.36 x 10(-6) (0.88 x 10(-6)) M, P=0.002). There was no s ignificant difference in nerve counts between the tissues, as assessed by s taining for acetylcholinesterase. Conclusions: Ulcerative colitis tissue has an increased sensitivity to carb achol and this is not due to denervation; it may result from increased calc ium release from intracellular stores since contraction due to membrane dep olarization is not altered. Modulation of this pathway could potentially be used to alter rectal motility in patients with ulcerative colitis.