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Impaired contractile response of mesenteric arteries in Crohn’s disease
Author(s) -
Lebuffe G.,
Haddad E.,
Desreumaux P.,
Gambiez L.,
Colombel J. F.,
Vallet B.
Publication year - 2000
Publication title -
alimentary pharmacology and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.308
H-Index - 177
eISSN - 1365-2036
pISSN - 0269-2813
DOI - 10.1046/j.1365-2036.2000.00838.x
Subject(s) - phenylephrine , medicine , mesenteric arteries , bradykinin , sodium nitroprusside , endocrinology , contraction (grammar) , vascular smooth muscle , vasodilation , crohn's disease , acetylcholine , artery , nitric oxide , disease , blood pressure , smooth muscle , receptor
Background: Crohn’s disease is associated with vascular injury and dysregulation of the intestinal immune system which together can provide disturbance of mesenteric circulation functional properties. Aim: To evaluate the vascular reactivity of mesenteric arteries from patients with Crohn’s disease. Methods: Phenylephrine‐induced contractions were assessed from 10 patients with Crohn’s disease and 8 control organ donors. N G ‐nitro‐ L ‐arginine‐methyl‐ester (L‐NAME) was used to test the presence of inducible NO synthase. Endothelium dependent and independent relaxation was assessed using acetylcholine, bradykinin, calcium ionophore A23187 and sodium nitroprusside. Results: The contractile response to phenylephrine was significantly decreased in arteries without endothelium from patients with Crohn’s disease. Exposure to the NO synthase inhibitor L‐NAME restored the contractile response to phenylephrine. Relaxation remained unaltered in both groups. Conclusion: These data provide direct evidence for fading of contraction caused by phenylephrine in Crohn’s disease. The restored mesenteric artery tone by a specific NO synthase inhibitor suggests that an increased production for NO in vascular smooth muscle might be responsible of this altered vascular reactivity.