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Propulsion in both small and large intestine is largely mediated by the peristaltic reflex; despite this, transit through the shorter colon is at least 10 times slower. Recently we demonstrated that elongating a segment of colon releases nitric oxide (NO) to inhibit peristalsis. The aims of this study were to determine if colonic elongation was physiologically significant, and whether elongation activated polarized intrinsic neural reflexes. Video imaging monitored fecal pellet evacuation from isolated guinea-pig colons full of pellets. Recordings were made from the circular muscle (CM) and longitudinal muscle (LM) in flat sheet preparations using either intracellular microelectrode or Ca 2+ imaging techniques. Full colons were 158.1 ± 6.1% longer than empty colons. As each pellet was expelled, the colon shortened and pellet velocity increased exponentially (full 0.34, empty 1.01 mm s −1 ). In flat sheet preparations, maintained circumferential stretch generated ongoing peristaltic activity (oral excitatory and anal inhibitory junction potentials) and Ca 2+ waves in LM and CM. Colonic elongation (140% of its empty slack length) applied oral to the recording site abolished these activities, whereas anal elongation significantly increased the frequency and amplitude of ongoing peristaltic activity. Oral elongation inhibited the excitation produced by anal elongation; this inhibitory effect was reversed by blocking NO synthesis. Pelvic nerve stimulation elicited polarized responses that were also suppressed by NO released during colonic elongation. In conclusion, longitudinal stretch excites specific mechosensitive ascending and descending interneurons, leading to activation of polarized reflexes. The dominance of the descending inhibitory reflex leads to slowed emptying of pellets in a naturally elongated colon.

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Small intestinal transit (SIT) has often been regarded as an index of pathophysiological state of postoperative ileus (PI) in rats. The reliability of SIT as an index of PI was examined in the present study. PI was induced via abdominal surgery (i.e., laparotomy with evisceration and manipulation) in rats. For one group of PI-induced rats, SIT of a charcoal test meal was measured. When necessary, the physical state (i.e., severity and site of distension) of the gastrointestinal (GI) tract in each rat was visually examined. For another group of PI-induced rats, abdominal X-ray radiographs were obtained after introducing the barium sulfate suspension. The abdomen was then opened and the physical state of the GI tract was visually examined. The SIT was decreased in most of the PI-induced rats, and the GI distension was observed, with substantial intersubject variations, in all of the PI-induced rats. However, no linear relationship was evident between the SIT and the severity of GI distension (e.g., at 20 h after PI induction). Instead, the severity and site of GI distension could be monitored by the X-ray radiology. Therefore, the use of SIT as an index of Pi should be substantially limited.

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