To determine the role of the diaphragm in the genesis of the high-pressure zone at the lower esophageal sphincter (LES) we studied the effect of diaphragmatic contraction on lower esophageal sphincter pressure in 10 anesthetized adult cats. Despite anchoring the pressure recording assembly within the LES to prevent axial movement of the sphincter during respiration relative to the pressure recording ports, there was an average oscillation in LES pressure of 17.4 ± 5.5 mmHg, the frequency of which was the same as the respiratory rate. Peak LES pressure occurred at end-inspiration corresponding with peak diaphragmatic electromyogram. During periods of central apnea induced by manual hyperventilation there was absence of both diaphragmatic electromyogram and the oscillations in LES pressure. Lower esophageal sphincter pressure during apnea was equal to end-expiratory pressure during spontaneous respiration. Following complete neuromuscular blockade with pancuronium, artificial respiration with increasing tidal volumes resulted in increasing oscillations in pressure. However, the magnitude of the pressure oscillation even at tidal volumes four times normal was always significantly below that observed during spontaneous eupnic respiration. Furthermore, progressive augmentation of diaphragmatic electromyogram activity by breathing 5% CO2 in air revealed a linear correlation between the magnitude of the respiratory-induced pressure oscillations of the LES and peak integrated diaphragmatic electromyogram in individual animals. It is concluded, therefore, that (a) intrinsic LES tone is best approximated by end-expiratory pressure during spontaneous respiration, (b) the respiratory-induced oscillations in LES pressure are primarily the result of active diaphragmatic contraction, and (c) the level of diaphragmatic electrical activity directly influences the magnitude of the pressure oscillation.
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