ABSTRACT
Previous manometric studies of esophageal fluid bolus transport in humans have generally ignored the hydrodynamic distinction between intrabolus pressure and pressure within the lumen-occluded, contracting esophageal segment. In this study we obtained concurrent esophageal videofluoroscopic and intraluminal manometric recordings in supine normal volunteers using different bolus volumes and viscosities and abdominal compression. Intrabolus pressure increased with bolus volume, viscosity, and abdominal compression. Esophageal diameter increased with larger bolus volumes, and this increase was correlated with increases in intrabolus pressure. Intrabolus pressure was highest in the bolus tail. Peak intraluminal pressures > 20 mmHg above basal intrabolus pressure almost invariably were associated with effective peristalsis, whereas values of this pressure differential < 20 mmHg frequently were associated with ineffective peristalsis and retrograde bolus escape. Intrabolus pressure can serve as an important indicator of the forces resisting peristaltic transport and the occurrence of ineffective bolus transport.
Subject(s)
Deglutition/physiology , Esophagus/physiology , Abdomen/physiology , Adult , Analysis of Variance , Biomechanical Phenomena , Fluoroscopy/methods , Humans , Male , Manometry , Middle Aged , Models, Biological , Peristalsis/physiology , Video RecordingABSTRACT
The aim of this study was to characterize lower esophageal sphincter (LES) longitudinal muscle contraction during changes in LES pressure in opossums. LES pressure was used as a marker of LES circular muscle contraction. Longitudinal muscle contraction was measured by strain gauge transducers. For precise placement of the strain gauge on the LES, the high-pressure zone was identified using a manometric-laser illumination technique. Measurements were made during 1) spontaneous LES pressure fluctuations, 2) LES pressure changes induced by pharmacological agents, and 3) LES relaxation induced by vagal nerve stimulation. These studies show that 1) spontaneous LES pressure fluctuations correlated with spontaneous changes in LES longitudinal muscle contraction; 2) pharmacologically induced contraction and relaxation of LES pressure correlated with contraction and relaxation of LES longitudinal muscle, respectively; 3) a close temporal relationship existed between changes in LES longitudinal muscle contraction and LES pressure that occurred spontaneously or were induced pharmacologically; and 4) vagal stimulation caused LES longitudinal muscle contraction and LES pressure relaxation. We propose that LES longitudinal muscle may play a role in the modulation of intraluminal LES pressure.
Subject(s)
Esophagogastric Junction/physiology , Muscle, Smooth/physiology , Animals , Bethanechol , Bethanechol Compounds/pharmacology , Esophagogastric Junction/anatomy & histology , Esophagogastric Junction/drug effects , Male , Muscle Contraction/drug effects , Muscle Contraction/physiology , Muscle Relaxation/physiology , Nitroprusside/pharmacology , Opossums , Pentagastrin/pharmacology , Vagus Nerve/physiologyABSTRACT
Our 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.
