Evidence in the literature reports motility abnormalities in patients with inflammatory bowel disorders. Many of the symptoms reported by patients derive from alteration in gut physiology. The mechanisms of this dysmotility are uncertain but different factors, either direct or indirect, of muscles and nerves can produce alteration of gut functions through the involvement of endocrine and neural networks.
We can summarize that entry of new ingesta into the colon during the postprandial period stimulates enteric mechanisms to initiate an excessive number of both high and low-amplitude propagating contractions. The decreased contractile function of the smooth muscle further helps acceleration of propulsion by decreasing segmental contractions and allowing forward movement of the colonic contents with-
Fig. 1. One hour multilumen manometric recording in patients with ileal pouch-anal anastomosis during fasting. Four recording ports were placed in the afferent ileal tract (I), three recording ports were in the pouch (P) and one in the proximal anal canal (IA). Phase II motor pattern was abruptly interrupted simultaneously in all the recording sites: it was replaced by MMC phase 1 -like motility for about 15 min. During this complete quiescent period, a phase III-like motor complex was recorded at the most proximal pouch level (P1): at the same time, relaxation of the internal anal sphincter occurs (IA). Phase II-like motil-ity and basal anal tone resumed simultaneously in all the recording channels out impediments. The anorectal region is characterized by increased sensitivity to distension and reduced compliance
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