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.

Chronic obstruction of the guinea pig ileum leads to distension and muscular hypertrophy, but how this affects passive biomechanical and nerve-mediated contractions and clearance known as peristaltic reflex is unclear. Ileum of controls had a diameter of 3.0 +/- 1.1 mm and a circular muscle thickness of 37.2 +/- 11.2 microns; 4 wk after placement of a nonconstricting Gore-Tex band, the ileum was distended to 10.0 +/- 0.19 mm, and its muscle had hypertrophied to 195.0 +/- 61.2 microns. Hypertrophied segments exceeded controls in capacity (e.g., 5.1 +/- 1.1 vs. 1.1 +/0 0.2 ml at 6 cm), compliance, and hysteresis. Threshold volumes and pressures that triggered the reflex were 3.3 +/- 1.3 ml and 3.1 +/- 0.01 mmHg in hypertrophied vs. 0.7 +/- 0.2 ml and 1.5 +/- 0.2 mmHg in controls. The diameter increase that triggered the reflex was 1.4 +/- 0.1 mm in hypertrophied segments and 0.6 +/- 0.1 mm in controls. Hypertrophied segments generated fewer contractions of virtually double the amplitude and failed to generate a pressure differential between up- and downstream sites as controls did. Hypertrophied segments generated larger stroke volumes and cumulative clearance than controls. The ratio of antegrade to retrograde clearance was similar in hypertrophied and control segments. The length of the occluding segment in hypertrophied preparations exceeded that of controls. Control contractions indented the antimesenteric border and propagated antegrade from their site of origin; bizarre writhing movements of hypertrophied segments made their contractions difficult to monitor. Thus distension and muscular hypertrophy do not interfere with the ability of the chronically obstructed guinea pig ileum to generate a peristaltic reflex at least as readily and as powerful and as effective in clearing the lumen as controls.

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Correlations were made between the adaptation of gastric pressure and longitudinal muscle tension. Isolated cat stomachs were filled with physiological solution and longitudinal strips marked in five segments over the lesser and the greater curvature (LC and GC). Strip length changed the most in the proximal segments of GC. Volume changes led to triphasic changes in gastric pressure. On filling, there was a pressure peak and pressure accommodation to a new base-line pressure. On emptying there was an initial pressure nadir that was followed by a pressure recovery. When isolated longitudinal strips were stretched and released to their lengths at specific gastric volumes, they generated triphasic tension adaption and recovery. Strips from the proximal greater curvature generated the highest base-line tension, highest peak tension, and largest amplitude of tension adaptations. Addition of KCl, carbachol, or physostigmine increased base-line tension and tension adaptations in parallel, whereas atropine reduced them. Tetrodotoxin had no effect. The base-line tension of the isolated cat stomach is maintained by a tonic cholinergic neurosecretion but its tension adaptations do not require neural control.

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