BACKGROUND: In past studies, investigators have reported that the salivary glands respond to esophageal acidification by increased salivary secretion and termed this response the 'esophago-salivary response'. The existence, however, of such a reflex was but a speculation because the verification of its mechanism could not be traced in the literature. In the current study, the hypothesis that the salivary glands' response to esophageal acidification is a reflex was investigated. METHODS: In 15 healthy volunteers (nine men, six women, age 32.3 +/- 4.2 years) the saliva of the four salivary glands was collected by intubation after individual esophageal perfusion with normal saline and 100 mmol HCl. The test was repeated after each of the lower esophagus and the salivary glands had been separately anesthetized. The latency was calculated. RESULTS: The mean basal volume of saliva was 62.7 +/- 6.4 mL/60 min. This volume did not show a significant change (P > 0.05) on esophageal saline instillation, whereas acid perfusion effected a significant increase (P < 0.01). The mean latency was 12.4 +/- 2.7 s. Esophageal acid perfusion after lower esophageal anesthetization did not produce a significant change in salivary volume; similar results were obtained on repetition of the test after anesthetization of salivary glands. When saline was used instead of lidocaine in the lower esophagus or salivary glands, the salivary glands' response was similar to that without saline perfusion. CONCLUSION: Esophageal acidification effected an increase of secreted saliva which clears the esophagus of the refluxed acid. Increased salivation on esophageal acidification is suggested to be a reflex and is mediated through the 'esophago-salivary' reflex. This reflex might be of diagnostic significance in the investigation of reflux esophagitis, a point that requires further study.
BACKGROUND: In past studies, investigators have reported that the salivary glands respond to esophageal acidification by increased salivary secretion and termed this response the 'esophago-salivary response'. The existence, however, of such a reflex was but a speculation because the verification of its mechanism could not be traced in the literature. In the current study, the hypothesis that the salivary glands' response to esophageal acidification is a reflex was investigated. METHODS: In 15 healthy volunteers (nine men, six women, age 32.3 +/- 4.2 years) the saliva of the four salivary glands was collected by intubation after individual esophageal perfusion with normal saline and 100 mmol HCl. The test was repeated after each of the lower esophagus and the salivary glands had been separately anesthetized. The latency was calculated. RESULTS: The mean basal volume of saliva was 62.7 +/- 6.4 mL/60 min. This volume did not show a significant change (P > 0.05) on esophageal saline instillation, whereas acid perfusion effected a significant increase (P < 0.01). The mean latency was 12.4 +/- 2.7 s. Esophageal acid perfusion after lower esophageal anesthetization did not produce a significant change in salivary volume; similar results were obtained on repetition of the test after anesthetization of salivary glands. When saline was used instead of lidocaine in the lower esophagus or salivary glands, the salivary glands' response was similar to that without saline perfusion. CONCLUSION: Esophageal acidification effected an increase of secreted saliva which clears the esophagus of the refluxed acid. Increased salivation on esophageal acidification is suggested to be a reflex and is mediated through the 'esophago-salivary' reflex. This reflex might be of diagnostic significance in the investigation of reflux esophagitis, a point that requires further study.