Lower oesophageal sphincter response to intravenous infusions of pentagastrin in normal subjects, antrectomised and achalasic patients.

Abstract

SUMMARY Lower oesophageal sphincter response to infusion of graded doses (0'003-0 050 ,ig kg-'min-') of pentagastrin was evaluated in four antrectomised patients as well as in six healthy subjects and seven achalasic patients in whom inhibition of antral gastrin release was maintained by continuous acidification (HCl 0 1 N) and aspiration of gastric antrum. In normal subjects and in antrectomised patients doses of pentagastrin required for half-maximal gastric acid secretion (0-012 p,g kg-'min-1) produced statistically significant increases of LES pressure. In achalasic patients, the infusion of pentagastrin did not affect LES pressure. These data seem to indicate that gastrin plays, at least in some degree, a physiological role in the regulation of LES tone. Insensitivity of LES to pentagastrin in achalasia suggests that the raised sphincter pressure in this disorder can not be attributed to gastrin.Gastrin and its analogue pentagastrin (PG) have been shown to increase lower oesophageal sphincter (LES) pressure (Giles et al., 1969;Castell and Harris, 1970). This effect has been reported to be enhanced in patients with achalasia (Cohen et al., 1971). Other studies, however, did not confirm these data (Farrell et al., 1974;Sturdevant and Kun, 1974;Goyal and McGuigan, 1976;Walker et al., 1975), and the role of the hormone in maintaining LES tone has yet to be determined.In previous investigations little consideration has been given to possible variations in endogenous serum gastrin levels during basal and stimulation periods. It might well be that variable endogenous serum gastrin levels interact at receptor sites with exogenous gastrin or pentagastrin, thus altering the resulting data. The aim of the present study was to evaluate the LES pressure response to graded doses of PG in subjects during maximal inhibition of antral gastrin release. Normal subjects and achalasic patients in whom the antral mucosa was continuously bathed with HCI 0'1 N solution MethodsSix normal volunteers (four males and two females), four male patients, previously operated upon for duodenal ulcer with antrectomy and gastrojejunal anastomosis, and seven achalasic patients (four males and three females), were investigated. Diagnosis of achalasia was made on the basis of radiological, endoscopic, and manometric findings. None of the normal and antrectomised subjects had symptoms related to the gastrointestinal tract and particularly clinical, radiological, and pH-manometric evidence of gastro-oesophageal reflux was lacking; none was taking drugs of any kind.Three water-filled, polyvinyl catheters, 1 mm internal diameter, were used to transmit intraluminal pressures to Elema-Sch6nander external transducers.Manometric variations were then recorded on a multichannel Hellige polygraph. The catheters had side openings, 1 2 mm in diameter, arranged to measure intraluminal pressures at three points, 5 cm apart. The pressure recording tubes were perfused with distilled water at a constant rate of 0 750 ml/min using a Braun syringe pump.Constant H...

Active and Inactive Gastroesophageal Reflux Diseases Related to Helicobacter pylori Therapy

“…However, when endogenous gastrin release was stimulated by calcium gluconate, ZES patients showed increased LES pressure [63]. Besides ZES, previous studies revealed that a high dose of pentagastrin, a gastrin analog, increased LES pressure, but a low dose of gastrin did not [65][66][67]. Whereas gastrin-I (gastrin-17), one of the physiological gastrins, gives a conflicting result, Heil et al and Jennewein et al reported that a high dose of gastrin-17 induced an increased LES pressure, as did pentagastrin [68,69].…”

Hormonal Control of Gastrointestinal Motility

“…In the early seventies, sev eral investigators demonstrated that bolus in jections of exogenous gastrin elevated the LES pressure [8,9], They suggested that gas trin may play a role in the regulation of LES competence. A number of studies employing physiological doses of exogenous gastrin and simultaneous measurement of LES pressure and plasma gastrin have not confirmed this initial study (10)(11)(12)(13).…”