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How the movements of the intestinal walls relate to luminal pressures and outflow remains incompletely understood. We triggered the peristaltic reflex in the isolated ileum of the guinea pig and quantified wall movements through computerized measurements of diameter changes. Contractions developed as indentations close to the upstream end of the loop. The indentations deepened and expanded in length. The downstream shoulder of contractions started and stopped to propagate before the upstream shoulder. Shoulders differed in their length and gradient over most of the duration of the contraction, and this gives the contraction an axial asymmetry. Over the course of individual contractions, the length of the indented segment correlated well with the luminal pressure. Contractions in response to large volumes generated long indented segments and high luminal pressures. The onset and the end of pressure waves and of outflow did not necessarily coincide with the onset and end of visual parameters of contractions. These findings indicate that objective visual parameters might be useful to describe and to classify contractions.

To understand how contractions move gastric contents, we measured, in isolated cat stomachs, the effects of contractions on gastric length, diameters, pressures, and emptying. Movements of the stomach and of gastric contents were monitored by video camera and ultrasound and were related to mechanical events. Based on pressures, we defined the following four phases of contractions: 1) Po, a steady pressure associated with tonic contraction of proximal stomach; 2) P′, a pressure wave during which the contraction indents the gastric body; 3) a pressure nadir while the contraction lifts the gastric sinus toward the incisura; and 4) a second pressure wave, P”, as the contraction advances through the antrum. In open preparations, liquid output and shortening of the greater curvature are large during Po, stop during P′, and resume with P”. Contractions generate higher pressures when gastric volume is held steady. Contractions increase wall thickness and decrease gastric diameters at sites they involve and have opposite effects at remote sites. Contractions move the incisura and hence redraw the borders between gastric segments and shift volumes back and forth within the gastric lumen. Contractions furthermore stir up, compress, and disperse particulate beans without moving them to the pylorus. We conclude that gastric contractions 1) reverse changes in gastric length that occur during gastric filling, 2) move gastric contents directly through local contact and indirectly by changing the configuration of the stomach, and 3) interact with structures such as the incisura in retaining and breaking up solid gastric contents.

We assessed how acute inflammation affects the contractile activity of the esophageal body. Two models of esophagitis were used: nine opossums had an esophageal perfusion of 100 meq hydrochloric acid for 2 hr and were studied at 24 hr. Ten had the perfusion for 4 h and their esophagitis were studied in vitro after 72 hr. Comparisons were made in all instances to animals who had esophageal saline perfusion for identical periods. All acid-perfused animals developed gross and histologic evidence of mucosal inflammation; in three animals, inflammatory changes extended into the submucosa and the muscularis propria. Manometric recordings in the acid-perfused animals revealed esophageal shortening, frequent failure of primary peristalsis and frequent occurrence of spontaneous contractions. Recordings of isometric tension of muscle in vitro revealed spontaneous contractions in strips from the mucosa and from the circular and from the longitudinal muscle. The amplitude of contractions in response to electrical stimulation was decreased, but the duration of contractions was increased largely because of a prolonged recovery phase. These changes in mechanical response occurred with stimulus parameters directed at both the muscle and the intrinsic nerves. We conclude that esophageal inflammation can lead to an increased irritability and decreased stimulus response of the smooth muscle of the esophagus even where it is not directly involved in an inflammatory response. These changes correspond to the functional abnormalities of the esophagus seen in patients with reflux esophagitis.