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Protective effect of trapencaine in acetic-acid-induced colitis in rats

  • Cell Injury and Protection in the Gastrointestinal Tract: from Basic Science to Clinical Perspectives 8–11 October 1995, Pécs, Hungary
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Abstract

Despite extensive research, the aetiology and pathogenesis of ulcerative colitis are still unknown and the therapeutic approach remains therefore empirical. Since trapencaine, a local anaesthetic, has been repeatedly demonstrated to protect the gastric mucosa from the injurious effects of a variety of noxious stimuli, its efficacy against acute inflammatory attack of the colonic mucosa was studied in a rat model of colitis induced by intracolonic administration of 4% acetic acid.

Vehicle or trapencaine in doses of 3, 10 and 30 mg/kg were given 30 min before acetic acid and the resulting injury was assessed after 48 h. Gross findings were ranked using the criteria of MacPherson and Pfeiffer. The length and wet/dry weight ratio of the colon were recorded, colonic fluid absorption was assessed and myeloperoxidase activity in colonic mucosal scrapings was determined. Contractility of colonic muscle strips was examined in vitro.

Trapencaine pretreatment was found to reduce the extent of the inflammatory colonic mucosal injury induced by acetic acid administration, as evidenced by the significant decrease in the rank of gross mucosal damage and in wet/dry colonic weight ratio, as well as by the attenuation of granulocyte infiltration. The increased responsiveness of colonic smooth muscle to acetylcholine and barium chloride associated with acute colitis was diminished by trapencaine pretreatment. The results indicate that trapencaine locally present in the colon seems to maintain the intregrity of colonic mucosa.

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Authors and Affiliations

  1. Institute of Experimental Pharmacology, Slovak Academy of Sciences, Bratislava, Slovak Republic

    V. Nosáĺová & V. Bauer

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  1. V. Nosáĺová
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  2. V. Bauer
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Nosáĺová, V., Bauer, V. Protective effect of trapencaine in acetic-acid-induced colitis in rats. Inflammopharmacology 4, 387–398 (1996). https://doi.org/10.1007/BF02755791

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  • DOI: https://doi.org/10.1007/BF02755791

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