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AJP - Gastrointestinal and Liver Physiology, Vol 259, Issue 2 306-G313, Copyright © 1990 by American Physiological Society
ARTICLES |
L. Marzio, P. Blennerhassett, S. Chiverton, D. L. Vermillion, J. Langer and S. M. Collins
Intestinal Diseases Research Unit, McMaster University Medical Centre, Hamilton, Ontario, Canada.
We have extended a recent study demonstrating increased contractility of jejunal smooth muscle of rats infected with the nematode parasite Trichinella spiralis, the primary habitat of which is the jejunum. In this study, muscle from the worm-free ileum of infected rats showed decreased contractility compared with control, illustrating regional differences in muscle responses to the infection. However, in jejunal muscle from worm-free segments that had been excluded from the rest of the gut before the infection, we observed increased tension generation, suggesting a systemic mechanism. To evaluate whether the changes in jejunal muscle were due to the host's inflammatory reaction, the effect of beta-methasone was examined. In a dose of 3.0 mg/kg sc daily, the steroid abolished the increase in myeloperoxidase activity associated with the infection and attenuated the increased tension generation in jejunal muscle from Trichinella-infected rats. These results support the hypothesis that alterations in intestinal smooth muscle function in this model do not require the presence of the parasite in the lumen and are mediated by the host's inflammatory reaction.
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