• J L Ren, W J Dodds, C J Martin, R O Dantas, R K Mittal, S S Harrington, M K Kern, and J G Brasseur.
• Department of Radiology, Medical College of Wisconsin, Milwaukee 53226.
• Am. J. Physiol. 1991 Sep 1;261(3 Pt 1):G417-25.

AbstractOur aim in this study was to determine the effect of variations in intrabolus pressure on esophageal peristalsis. In five cats, intrabolus pressure was altered by increasing intragastric pressure to 20-45 mmHg by use of a pressure cuff to compress the abdomen. In each cat, increases in intragastric pressure were associated with comparable increases in pressure of the esophageal bolus while the bolus was in the distal esophagus during esophageal peristalsis. Secondary peristalsis induced by a 5-ml injection of barium into the proximal esophagus was recorded by synchronized videofluoroscopy and esophageal manometry. Graded increases in intrabolus pressure caused an increased prevalence of ineffective, incomplete peristaltic sequences that did not completely clear barium from the esophagus. At intragastric pressures greater than 45 mmHg, 63% of the peristaltic sequences were incomplete. Increases in intrabolus pressure elicited by increased intragastric pressure also caused 1) slowing of the peristaltic wave in the distal esophagus, 2) increased pressure wave duration in the distal esophagus, 3) increased esophageal diameter, and 4) increased duration of lower esophageal sphincter opening. The incidence of retrograde bolus escape was inversely related to the difference between peristaltic wave amplitude and intrabolus pressure. A pressure difference of greater than 20 mmHg prevented retrograde barium escape at all esophageal levels, whereas a difference of less than 20 mmHg was generally associated with retrograde escape of barium in the distal esophagus. We conclude that an increase in intrabolus pressure causes an increase in esophageal distension that is transduced into alterations of esophageal peristalsis by either a myogenic or neural mechanism.

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