Functional motor changes and morphological alterations have been associated with intestinal inflammation. The aim of our study was to evaluate functional alterations of intestinal reflexes and of the responses to CCK in the Trichinella spiralis model of intestinal inflammation. Rats were prepared with strain gauges and electrodes in the small intestine to evaluate spontaneous motor activity, the ascending contraction of the peristaltic reflex, and the motor responses to CCK-8 infusion. Infected animals showed increased motor activity at the duodenum and jejunum but not at the ileum. Ascending contraction was increased in both duodenum and ileum. Ascending excitation after N(omega)-nitro-L-arginine was still increased as well as the residual response after atropine. Response to CCK-8 during intestinal inflammation was changed in the jejunum, in which it turned from the inhibition shown in healthy animals to excitation. NADPH-diaphorase staining did not show any changes between distribution and density of positive neurons in either healthy or infected animals. In conclusion, intestinal inflammation induces functional changes in the motor activity that could explain the abnormal motor responses observed in inflammatory disorders.

Nerve growth factor (NGF) could be involved in the development of hyperalgesia as well as in nervous remodeling consequence of inflammation. Both dysmotility and increase of visceral sensitivity have been described in functional gastrointestinal disorders such as irritable bowel syndrome. Trichinella spiralis-infected rats show an exacerbated spontaneous motility and a significant increase of the excitatory response to cholecystokinin (CCK), both associated with a reversible inflammatory process and the hypertrophy of the muscle layers. In this study we determined the intestinal expression of NGF mRNA by polymerase chain reaction and NGF by enzyme-linked immunosorbent assay. We implanted serosal strain gauge transducers on duodenum, jejunum, and ileum of anesthetized Sprague-Dawley rats to record circular muscle contractions. The experimental protocol included the evaluation of intestinal spontaneous motor activity (SMA), the response to CCK-8, and the ascending contraction induced by electrical mucosal stimulation. This protocol was performed in healthy and infected nontreated rats, in healthy rats with an NGF antibody treatment (1.6 mg/rat i.p.), and in infected rats with the same treatment applied at 0 or 3 days postinfection. NGF and NGF mRNA levels in the bowel were increased during inflammation. Although anti-NGF treatments did not prevent or reverse inflammatory response, the treatment was effective in preventing the motor alterations induced by the T. spiralis infection, i.e., inhibited increased SMA, reversed altered response to CCK, and reversed in part exacerbated response to electrical stimulation.

Trichinella spiralis infection in rodents is a well-known model of intestinal inflammation associated with hypermotility and hypersecretion. Our aim was to use this experimental model to elucidate if iNOS was involved in the development of gastrointestinal hypermotility. Rats infected with Trichinella spiralis were treated for 4 days with the nitric oxide synthase inhibitors L-NAME or L-NIL. Treatment began either simultaneously with the infection or 3 days after infection when inflammation was already fully developed. In all cases, at day 10-12 after infection, anesthetized rats were prepared with strain gauges and electrodes in the small intestine to evaluate motor activity of the small intestine. In addition, histology and iNOS immunohistochemistry studies were performed. The results showed that both NOS inhibitors blocked iNOS expression in the intestine. None of the NOS inhibitors attenuated the inflammatory process. However, the preventive treatment with L-NIL reversed hypermotility. In contrast, the treatment with NOS inhibitors 3 days after infection was not so effective in reversing motor alterations. L-NAME, but not L-NIL, caused alterations on spontaneous motility. In conclusion, these results indicate that iNOS participates in the development of motor hypermotility in the gut.

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