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Neural mechanisms of early postinflammatory dysmotility in rat small intestine.
Neurogastroenterol Motil 2006; 18(12):1102-11NM

Abstract

Although human postinflammatory dysmotility is known, so far animal studies have primarily investigated changes during inflammation. Here, we focused on postinflammatory changes in rat jejunal myenteric plexus and jejunal motility. Evolution of ethanol/2,4,6-tri-nitrobenzene sulphonic acid (TNBS)-induced inflammation was assessed histologically and by measuring myeloperoxidase activity (MPO). Electromyography and immunohistochemistry were performed 1 week after ethanol/TNBS and also after N(G)-nitro-L-arginine methyl ester (L-NAME) administration. Ethanol/TNBS induced a transient inflammation, with normalization of MPO and histological signs of an early phase of recovery after 1 week. The number of cholinergic neurones was not altered, but myenteric neuronal nitric oxide synthase (nNOS)-immunoreactivity was significantly lower in the early phase of recovery after TNBS compared with water (1.8 +/- 0.2 vs 3.5 +/- 0.2 neurones ganglion(-1), P < 0.001). Interdigestive motility was disrupted with a loss of phase 1 quiescence, an increase of migrating myoelectric complex cycle length, a higher number of non-propagated activity fronts and a decrease of adequately propagated phase 3 s after TNBS. Administration of L-NAME resulted in a similar disruption of interdigestive motility patterns. In the early phase of recovery after ethanol/TNBS-induced jejunal inflammation, a loss of motor inhibition occurs due to a decrease of myenteric nNOS activity. These observations may provide a model for early postinflammatory dysmotility syndromes.

Authors+Show Affiliations

Center for Gastroenterological Research, Catholic University Leuven, Leuven, Belgium.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

17109694

Citation

Demedts, I, et al. "Neural Mechanisms of Early Postinflammatory Dysmotility in Rat Small Intestine." Neurogastroenterology and Motility : the Official Journal of the European Gastrointestinal Motility Society, vol. 18, no. 12, 2006, pp. 1102-11.
Demedts I, Geboes K, Kindt S, et al. Neural mechanisms of early postinflammatory dysmotility in rat small intestine. Neurogastroenterol Motil. 2006;18(12):1102-11.
Demedts, I., Geboes, K., Kindt, S., Vanden Berghe, P., Andrioli, A., Janssens, J., & Tack, J. (2006). Neural mechanisms of early postinflammatory dysmotility in rat small intestine. Neurogastroenterology and Motility : the Official Journal of the European Gastrointestinal Motility Society, 18(12), pp. 1102-11.
Demedts I, et al. Neural Mechanisms of Early Postinflammatory Dysmotility in Rat Small Intestine. Neurogastroenterol Motil. 2006;18(12):1102-11. PubMed PMID: 17109694.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Neural mechanisms of early postinflammatory dysmotility in rat small intestine. AU - Demedts,I, AU - Geboes,K, AU - Kindt,S, AU - Vanden Berghe,P, AU - Andrioli,A, AU - Janssens,J, AU - Tack,J, PY - 2006/11/18/pubmed PY - 2007/1/11/medline PY - 2006/11/18/entrez SP - 1102 EP - 11 JF - Neurogastroenterology and motility : the official journal of the European Gastrointestinal Motility Society JO - Neurogastroenterol. Motil. VL - 18 IS - 12 N2 - Although human postinflammatory dysmotility is known, so far animal studies have primarily investigated changes during inflammation. Here, we focused on postinflammatory changes in rat jejunal myenteric plexus and jejunal motility. Evolution of ethanol/2,4,6-tri-nitrobenzene sulphonic acid (TNBS)-induced inflammation was assessed histologically and by measuring myeloperoxidase activity (MPO). Electromyography and immunohistochemistry were performed 1 week after ethanol/TNBS and also after N(G)-nitro-L-arginine methyl ester (L-NAME) administration. Ethanol/TNBS induced a transient inflammation, with normalization of MPO and histological signs of an early phase of recovery after 1 week. The number of cholinergic neurones was not altered, but myenteric neuronal nitric oxide synthase (nNOS)-immunoreactivity was significantly lower in the early phase of recovery after TNBS compared with water (1.8 +/- 0.2 vs 3.5 +/- 0.2 neurones ganglion(-1), P < 0.001). Interdigestive motility was disrupted with a loss of phase 1 quiescence, an increase of migrating myoelectric complex cycle length, a higher number of non-propagated activity fronts and a decrease of adequately propagated phase 3 s after TNBS. Administration of L-NAME resulted in a similar disruption of interdigestive motility patterns. In the early phase of recovery after ethanol/TNBS-induced jejunal inflammation, a loss of motor inhibition occurs due to a decrease of myenteric nNOS activity. These observations may provide a model for early postinflammatory dysmotility syndromes. SN - 1350-1925 UR - https://www.unboundmedicine.com/medline/citation/17109694/Neural_mechanisms_of_early_postinflammatory_dysmotility_in_rat_small_intestine_ L2 - https://doi.org/10.1111/j.1365-2982.2006.00857.x DB - PRIME DP - Unbound Medicine ER -