Alteration of intestinal myoelectrical activity is a characteristic feature of food protein-induced intestinal anaphylaxis in the conscious rat. The motility changes induced by antigen challenge were appraised in egg-albumin-sensitized rats, chronically implanted with NiCr electrodes in the duodenojejunal wall. Intraduodenal infusion of egg albumin given to fasted sensitized rats triggered a disruption of the cyclic pattern of small intestinal motility lasting 79.1 ± 23.3 min. The duration of the challenge effect on intestinal myoelectrical activity was significantly reduced by systemic capsaicin pretreatment (125 mg/kg) but to a lesser extent by perivagal capsaicin. Substance P (SP) antagonists (SP 4-11 and CP 96.345) and atropine were also able to shorten the duration of the antigen-challenge-induced alteration of intestinal motility. It is concluded that SP and capsaicin-sensitive afferent nerve endings play an important role in the intestinal anaphylaxis-induced disturbances of intestinal motility.

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Two micrograms of prostaglandin E2 injected into the lateral ventricle of the brain in rats had the same anorectic and gastrointestinal motor effect as central administration of 0.02 unit of calcitonin. The effects of calcitonin were blocked by a previous intracerebroventricular administration of 0.25 milligram of indomethacin. These results suggest that both anorectic and gastrointestinal motor effects of calcitonin are centrally mediated by the release of prostaglandins.

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