title: Alterations in intestinal contractility during inflammation are caused by both smooth muscle damage and specific receptor-mediated mechanisms.
abstract: OBJECTIVE
  To evaluate motoric intestinal disturbances during inflammation with Trichinella spiralis in rats as an experimental model.
  
  
  METHODS
  We examined the changes in worm-positive (jejunum) and worm-free (ileum) intestinal segments of rats infected with T. spiralis. To investigate the relationship between structural and functional changes in smooth muscle, we measured the thickness of the muscle layers of rat jejunum and ileum. Mechanical responses to KCl 30 mmol/L, acetylcholine (ACh) 10(-8)-10(-4) mol/L, substance P (SP) 10(-9)-10(-5) mol/L, and to electrical field stimulation of longitudinal muscle strips in the jejunum and ileum were studied in muscle bath as controls (day 0) and on day 2, 6, 14, 23, and 72 after infection.
  
  
  RESULTS
  After T. spiralis infestation, an inflammation of the mucosal and submucosal layers of jejunum was observed, whereas in the worm-free ileum there was not any inflammatory infiltrate. Increase in the smooth muscle thickness of both jejunum and ileum were correlated with increased responses to depolarizing agent KCl and to ACh. However, responses to SP were decreased on day 14-23 after infection in jejunum and from day 6-14 after infection in ileum. Electric field stimulation-induced contractions were transiently decreased in the jejunum (day 2 after infection) but in the ileum the contractile responses were decreased until the end of the study period.
  
  
  CONCLUSIONS
  Alterations in intestinal smooth muscle function do not require the presence of the parasite and the absence of histopathological signs of inflammation do not warrant intact motor function. Changes in motor responses after T. spiralis infection are not only due to smooth muscle damage but also to disturbances in specific receptor-mediated mechanisms.
authors.affiliation: Department of Physiology, Veterinary Faculty of Sarajevo, Sarajevo, Bosnia and Herzegovina. atanovic@pharmamar.com
authors.forename: Adnan
authors.initials: A
authors.lastname: Tanović
authors.forename: Ester
authors.initials: E
authors.lastname: Fernández
authors.forename: Marcel
authors.initials: M
authors.lastname: Jiménez
mesh_terms: D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D004558:Electric Stimulation; D005769:Gastrointestinal Motility; D066298:In Vitro Techniques; D007249:Inflammation; D007421:Intestine, Small / Q000469:parasitology / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000473:pathology / Q000503:physiopathology*; D018377:Neurotransmitter Agents / Q000494:pharmacology; D011189:Potassium Chloride / Q000494:pharmacology; D051381:Rats; D017207:Rats, Sprague-Dawley; D013373:Substance P / Q000494:pharmacology; D017160:Trichinella spiralis; D014235:Trichinellosis / Q000469:parasitology / Q000473:pathology / Q000503:physiopathology*
chemical_list: D018377:Neurotransmitter Agents; D013373:Substance P; D011189:Potassium Chloride; D000109:Acetylcholine