Antibiotic depression of evoked and spontaneous responses of opossum distal colonic muscularis mucosae in vitro: a factor in antibiotic-associated colitis?
Certain antibiotics depress both skeletal neuromuscular transmission and intestinal neuroeffector transmission. Impaired intestinal motility may facilitate the proliferation of the bacterium Clostridium difficle and thus lead to the development of antibiotic-associated pseudomembranous colitis. Many antibiotics accumulate in the colonic lumen at concentrations several times their associated blood levels. This study examined whether certain of these could interfere with colonic muscularis mucosal movement in vitro, using tissue from opossum distal colon as a model. At concentrations approximating those in the colonic lumen, ampicillin, clindamycin, erythromycin, and lincomycin depressed tone and spontaneous contractions of the muscularis mucosae. Clindamycin, gentamicin, kanamycin, and lincomycin abolished electrically evoked contractions but only gentamicin and kanamycin could abolish the ensuing relaxation. Vancomycin potentiated the response of the muscularis mucosae to acetylcholine; erythromycin and clindamycin depressed it. Antibiotic-induced depression of colonic muscularis mucosal movement may contribute to the development of antibiotic-associated pseudomembranous colitis.[1]References
- Antibiotic depression of evoked and spontaneous responses of opossum distal colonic muscularis mucosae in vitro: a factor in antibiotic-associated colitis? Percy, W.H., Christensen, J. Gastroenterology (1985) [Pubmed]
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