Stimulation of the incompetent lower esophageal sphincter. A possible advance in therapy of heartburn.
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Biomedical subjects
Publications and source records attributed to D O Castell.
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Lower oesophageal sphincter pressure has been studied in pernicious anaemia patients and controls using an infused open-tipped system. Resting sphincter pressure was significantly (p < 0.01) lower in the pernicious anaemia patients. After gastric acidification with 0.1 N HCl pressure fell significantly (p < 0.01) in both groups. Following subsequent alkalinization, lower oesophageal sphincter pressure for controls rose significantly (p < 0.001). For pernicious anaemia patients the pressure after alkali was not greater than resting levels. Graded intravenous doses of pentagastrin in controls resulted in a peak pressure change of 38.5 +/- 4.9 mm Hg after the 0.8 mug/kg dose. For patients the peak pressure change was only 13.0 +/- 5.2 mm Hg and occurred after 0.4 mug/kg. Cholinergic stimulation with edrophonium (10 mg) produced a peak pressure change of 20.6 +/- 2.6 mm Hg in controls but only 3.5 +/- 1.0 mm Hg in pernicious anaemia patients (p < 0.001). In addition, no change in lower oesophageal sphincter pressure occurred in patients after stimulation with subcutaneous betazole (1.5 mg/kg). In conclusion, the lower oesophageal sphincter in pernicious anaemia is characterized both by a low resting pressure and a decreased response to endogenous and exogenous stimuli. These results suggest a primary end organ defect and most likely indicate abnormal smooth muscle function in pernicious anaemia. Resting sphincter pressure levels and edrophonium response in age-matched subjects indicate that these changes are not due to aging alone.
The effect of fat and protein meals on the lower oesophageal sphincter pressure was tested in normal subjects using an infused open-tipped manometric system. After ingestion of a minced beef meal, the mean peak pressure at the lower oesophageal sphincter increased 5.8 +/- 1.5 mm Hg (+/- 1 SE). By contrast, ingestion of a corn oil meal resulted in a mean peak decrease of 7.8 +/- 1.9 mm Hg. Following the combined minced beef/corn oil meal, mean peak pressure decreased 3.0 +/- 2.1 mm Hg. Pentagastrin (3 mug/kg, subcutaneously) resulted in a mean peak increase of 20.6 +/- 7.0 mm Hg when given to the subjects in the fasting state, and produced an increase of only 8.4 +/- 1.7 mm Hg when given following the fat meal. Finally, after a mean peak decrease in pressure at the lower oesophageal sphincter of 6.8 +/- 1.0 mm Hg 15 minutes after the corn oil meal, gastric alkalinization with 30 ml of antacid resulted in a subsequent increase in sphincter pressure of 5.2 +/- 1.6 mm Hg. These data indicate: (1) Fat attenuates the effect of endogenous gastrin as well as exogenous pentagastrin stimulation of the lower oesophageal sphincter. (2) Fat-induced incompetency of the lower oesophageal sphincter can be effectively combated by gastric alkalinization in the form of antacids.
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