Pathogenesis of lower-esophageal-sphincter incompetence.
作者： W. H. Lipshutz , R. D. Gaskins , W. M. Lukash , J. Sode
DOI: 10.1056/NEJM197307262890404
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摘要: Abstract Since patients with symptomatic gastroesophageal reflux have diminished lower-esophagealsphincter pressure, we studied the pathogenesis of this sphincteric pressure. In 23 as compared to 20 controls, lower-esophageal-sphincter response direct muscle stimulation by a parasympathomimetic drug (beth-anechol chloride) and effect cholinesterase inhibitor (edrophonium was identical. Complete dose-response curves pressure exogenous intravenous pentagastrin were also similar in both groups. The endogenous gastrin release patients. Pressure (mean ± S.E.) increased gastric deacidification subjects 1.5 0.5 mm Hg (70.5 3.6 per cent) 10.5 (197.5 11.6 controls (p<0.001). infusion glycine 2.3 (35.7 5.0 19.4 3....
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