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AJP - Gastrointestinal and Liver Physiology, Vol 255, Issue 6 701-G708, Copyright © 1988 by American Physiological Society
ARTICLES |
D. L. Vermillion, P. B. Ernst, R. Scicchitano and S. M. Collins
Intestinal Diseases Research Unit, McMaster University, Hamilton, Ontario, Canada.
We examined contractility of longitudinal muscle strips of jejunum from control rats and rats infected 34-85 days previously with Trichinella spiralis. Antigen prepared from T. spiralis larvae contracted muscle from previously infected but not control rats. Contraction was specific for the sensitizing agent because antigen from Nippostrongylus brasiliensis did not induce contraction. Contraction was resistant to atropine or tetrodotoxin but was inhibited by the 5-hydroxytryptamine (5-HT) antagonist cyproheptadine and by 5-HT desensitization. Neither histamine antagonists, diphenhydramine (H1-receptor antagonist) or ranitidine (H2-receptor antagonist), nor indomethacin, a prostaglandin synthase inhibitor, influenced the antigen response. In Trichinella-infected rats there was a significant increase in mast cell number in the muscle layers, and the contraction induced by T. spiralis antigen was inhibited by the mast cell stabilizer doxantrazole. In addition, anti-rat immunoglobulin E serum, compound 48/80, and concanavalin A each contracted muscles from rats previously infected with T. spiralis. These results are consistent with the hypothesis that T. spiralis infection leads to mast cell proliferation in the muscle layers and that subsequent exposure to antigen results in mast cell degranulation, 5-HT release, and contraction of smooth muscle.
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