Physiology and pathophysiology of the lower esophageal sphincter.
The physiologic factors controlling lower esophageal sphincter (LES) function are interrelated in a complex fashion and include the autonomic nerve supply, gastrointestinal hormones, and specific characteristics of the circular smooth muscle at the esophagogastric junction. It might be expected that a defect in any of these three controlling mechanisms would result in a clinically recognizable symptom complex. Abnormalities with either high or low LES pressure have been shown to relate to these specific aspects. Studies of the effects of various foods and other agents which decrease or increase LES pressure are of therapeutic interest in relating to patients with reflux symptoms. Decreases in LES pressure occurring after fat ingestion may explain a mechanism for many cases of fatty food intolerance. Pressure decreases after chocolate ingestion, after smoking, and after alcohol all have strong therapeutic implications in patients with chronic heartburn. Gastric alkalinization will increase pressure for up to one hour in patients with basal sphincter hypotension and reflux symptoms. Recent studies with drugs that work through the cholinergic mechanism have important therapeutic considerations. Anticholinergic agents produce definite decreases in LES pressure and are to provided in treatment of patients with reflux symptoms. On the other hand cholinergic drugs such as bethanechol have been shown to increase LES pressure in normal subjects and in patients with chronic sphincter incompetence. Recently, a double-blind therapeutic trial with bethanechol in patients with chronic heartburn has indicated that this drug, when given on regular basis, is an effective adjunct to therapy in these patients.
D000752:Anemia, Pernicious / Q000503:physiopathology; D004032:Diet / Q000009:adverse effects; D004931:Esophageal Achalasia / Q000503:physiopathology; D004935:Esophageal Diseases / Q000209:etiology*; D004943:Esophagogastric Junction / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*; D005764:Gastroesophageal Reflux / Q000188:drug therapy / Q000503:physiopathology; D005768:Gastrointestinal Hormones / Q000502:physiology*; D006356:Heartburn / Q000188:drug therapy / Q000209:etiology; D006801:Humans; D008688:Methacholine Compounds / Q000627:therapeutic use; D009119:Muscle Contraction / Q000187:drug effects; D009130:Muscle, Smooth / Q000502:physiology*; D010276:Parasympatholytics / Q000494:pharmacology; D010277:Parasympathomimetics / Q000494:pharmacology; D012595:Scleroderma, Systemic / Q000503:physiopathology; D015043:Zollinger-Ellison Syndrome / Q000503:physiopathology
D005768:Gastrointestinal Hormones; D008688:Methacholine Compounds; D010276:Parasympatholytics; D010277:Parasympathomimetics