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1 Chaim Sheba Medical Center, Tel Hashomer, Israel; 2 First Teaching Hospital, Beijing Medical University, Beijing, China; and 3 Medical College of Wisconsin Dysphagia Institute, Division of Gastroenterology and Hepatology, Departments of Medicine, Radiology, and Otolaryngology, Medical College of Wisconsin, and Zablocki Department of Veterans Affairs Medical Center, Milwaukee, Wisconsin 53226
Recent studies have shown that afferent signals originating from the pharynx inhibit progression of primary esophageal peristalsis. Our aim was to further elucidate the effect of esophageal and pharyngeal afferent stimulation on primary and secondary esophageal peristalsis. We studied the effect of esophageal air distension and pharyngeal water stimulation on progression of primary and secondary peristalsis in nine healthy volunteers aged 27 ± 2 yr (4 men, 5 women). At a threshold volume, rapid injection of water into the pharynx, directed posteriorly, resulted in complete halt of the progressing secondary and primary esophageal peristalses in both the proximal and distal esophagus. The threshold volume of injected water for inducing inhibition was similar for secondary (0.6 ± 0.2 ml) and primary (0.5 ± 0.1 ml) esophageal peristalsis. Progression of primary peristalsis induced by a dry swallow and secondary peristalsis induced by intraesophageal air distension were completely inhibited by intraesophageal injection of 15 ± 2 ml of air in 70% and 75% of the trials, respectively. We conclude that afferent signals induced by esophageal air distension and pharyngeal water stimulation inhibit propagation of both primary and secondary esophageal peristalsis, suggesting a shared neural control mechanism for these types of peristalsis.
peristaltic inhibition; esophageal afferents; pharyngeal afferents; esophageal dysmotility
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