{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,12,14]],"date-time":"2025-12-14T15:54:35Z","timestamp":1765727675098,"version":"3.48.0"},"reference-count":42,"publisher":"BMJ","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Gut"],"published-print":{"date-parts":[[1993,3]]},"abstract":"<jats:p>The determinants of the oesophageal alkaline pH environment are poorly understood. Saliva (pH 6.4-7.8) may be a major contributor, although some argue the importance of refluxed alkaline duodenal contents. Acid and alkaline reflux parameters were studied over 2 days in 30 subjects (control, oesophagitis and Barrett's patients; 10 each) using glass pH electrodes. In phase 1, one pH electrode was placed 1 cm below the upper oesophageal sphincter to assess the influence of saliva and the other 5 cm above the lower oesophageal sphincter. Phase 2 was identical except that one pH probe was 5 cm below the lower oesophageal sphincter to record duodenogastric reflux. Patient groups spent, on average, 50 fold more time during the upright and supine periods at acidic pH than controls. Saliva was responsible for the percentage of time the pH &gt; 7 and contributed significantly to the percentage of time the pH &gt; 6 in both the proximal and distal oesophagus of control subjects, as shown by an absence of pH &gt; 7 and a significant (p &lt; 0.001) fourfold decrease in pH &gt; 6 during sleep. A similar pattern was seen in the proximal oesophagus of both reflux groups. The reflux and Barrett's patients, however did not show a significant decrease in the percentage of time the pH &gt; 6 at night in the distal oesophagus suggesting a relative increase in 'alkaline' exposure from another source. This was not because of duodenogastric reflux as the corresponding pH rises in the fundus of the stomach were non-existent. Although this was not studied specifically, it is believed to be a protective meachanism, the result of alkaline secretion produced by submucosal oesophageal glands.<\/jats:p>","DOI":"10.1136\/gut.34.3.309","type":"journal-article","created":{"date-parts":[[2007,9,18]],"date-time":"2007-09-18T17:41:31Z","timestamp":1190137291000},"page":"309-316","source":"Crossref","is-referenced-by-count":81,"title":["Determinants of oesophageal 'alkaline' pH environment in controls and patients with gastro-oesophageal reflux disease."],"prefix":"10.1136","volume":"34","author":[{"given":"S","family":"Singh","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"L A","family":"Bradley","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"J E","family":"Richter","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"239","published-online":{"date-parts":[[1993,3,1]]},"reference":[{"key":"ref_1","first-page":"276","article-title":"Role of components of gastroduodenal contents in experimental acid esophagitis","volume":"92","author":"Lillemoe, K.D.; Johnson, L.F.; Harmon, J.W.","year":"1982","unstructured":"Lillemoe KD, Johnson LF, Harmon JW. 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