Central action of interleukin 1 beta on intestinal motility in rats: mediation by two mechanisms.

Abstract

Interleukin 1 (IL-1) can influence gut functions by inhibiting gastric acid secretion. This study was performed to investigate the effects of IL-1 on intestinal motility and the mechanisms involved. The effects of IL-1 beta were determined by electromyography in conscious rats with implanted electrodes and a permanent catheter in a lateral brain ventricle. Intracerebroventricular IL-1 beta (15 ng) administered to fed rats immediately stimulated cecocolonic spike bursts and caused a migrating myoelectric complex pattern after a delay in the small intestine. Tenfold higher doses of peripherally administered IL-1 beta did not promote similar reactions. The IL-1 antagonist reduced the small intestinal effect of IL-1 beta and blocked the cecocolonic stimulation. Indomethacin and SC 19220 reduced the small intestinal effects but did not antagonize the increase in cecocolonic contractions. In contrast, alpha-helical CRF9-41 blocked the increase of cecocolonic contractions but did not antagonize the IL-1 beta-induced effects on the small intestine. IL-1 beta's effects on intestinal motility can be mainly ascribed to a central action. The cecocolonic stimulation may be mediated by brain corticotropin-releasing factor, whereas the small intestinal effects involve a prostaglandin mediation.