Effect of continuous infusion of pentagastrin on lower esophageal sphincter pressure and gastric acid secretion in normal subjects.

Walker, Charles O.; Frank, S.; Manton, J.; Fordtran, John S.

doi:10.1172/jci108070

Cited by 25 publications

(6 citation statements)

References 14 publications

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“…The role of gastrin in the physiologic regulation of lower esophageal sphincter pressure (LESP)' is controversial (1)(2)(3)(4)(5)(6)(7)(8). Some observers have proposed that circulating gastrin (3,4) is the major determinant of LESP.…”

Section: Introductionmentioning

confidence: 99%

Is gastrin a major determinant of basal lower esophageal sphincter pressure? A double-blind controlled study using high titer gastrin antiserum.

Goyal¹,

McGuigan²

1976

J. Clin. Invest.

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A B S T R A C T Studies were performed in anesthetized opossums to determine the influence of binding of circulating gastrin with a high titer gastrin antiserum on lower esophageal sphincter pressure. Gastrin antiserum or control antiserum was administered intravenously in successive doses of 0.02, 0.1, and 0.5 ml/kg on separate days. The lower esophageal sphincter pressures were measured for 1 h before and for 1 h after antiserum administration. The control serum caused no binding of opossum circulating gastrin, nor did it modify lower esophageal sphincter pressure. On the other hand, the administration of gastrin antiserum resulted in the binding of 85-90% of circulating gastrin, but it did not reduce sphincter pressure. A continuous infusion of 0.25 ,*g.kg'-h' of synthetic human gastrin I caused a significant (P <0.05) increase in the sphincter pressure, a 30-fold increase in gastric acid output, and a fourfold increase in immunoreactive gastrin in the opossum blood. Prior treatment with 0.1 ml/kg of gastrin antiserum antagonized and 0.2 ml/kg of the antiserum abolished the gastrin-stimulated gastric acid secretion and the stimulating effect of gastrin on lower esophageal sphincter pressure. However, neither dose of antiserum modified basal lower esophageal sphincter pressure. It is concluded that circulating gastrin may not be an important determinant of basal sphincter pressure.

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Section: Introductionmentioning

confidence: 99%

Is gastrin a major determinant of basal lower esophageal sphincter pressure? A double-blind controlled study using high titer gastrin antiserum.

Goyal¹,

McGuigan²

1976

J. Clin. Invest.

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“…The demonstrations that human LOS pressure could be modified by gastric infusions of acid and alkali (Castell and Harris, 1970;Beiles et al, 1972;Castell and Levine, 1972;Higgs et al, 1974); that LOS pressure could be consistently increased by gastrin and pentagastrin (Giles et al, 1969;Castell and Harris, 1970;Cohen and Lipshutz, 1971;Lipshutz et al, 1973;Siewert et al, 1974;Trindade et al, 1975); and that LOS pressure in the opossum could be drastically diminished by the use of gastrin antiserum (Lipshutz, et al, 1972) led to the proposal that gastrin was of primary importance in the regulation of LOS pressure. Recent studies, however, have cast considerable doubt upon the physiological relevance of gastrin in this context (Grossman, 1973;Sturdevant and Kun, 1973;Farrell et al, 1974;Goyal and McGuigan, 1975;Walker et al, 1975).…”

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confidence: 99%

Responses of the competent and incompetent lower oesophageal sphincter to pentagastrin and abdominal compression.

Kaye¹,

Rein²,

Johnson³

et al. 1976

Gut

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The central role of the physiological lower oesophageal sphincter (LOS) in the prevention of gastro-oesophageal reflux is now well recognised; and, in recent years, the effects upon resting LOS pressure of a number of hormones and drugs have been defined (Castell, 1975). However, the physiological means by which resting pressure within the LOS is maintained and modulated have not been fully elucidated; nor have the factors responsible for sphincteric incompetence, and therefore gastro-

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“…Walker et al (1975) reported that there was no statistically significant increase in LES pressure during PG infusion at doses of 0M004-12 ,ug kg-lh-1; however, examination of individual results suggested that PG might be stimulating LES pressure in some subjects and inhibiting it in others. Two further studies Kaye et al, 1976) showed that LES pressure increased during continuous infusion of PG at above maximal ( jig kg-lh-1) or submaximal (09 kg kg-lh-1) doses for gastric acid secretion in man.…”

Section: Discussionmentioning

confidence: 97%

“…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.…”

mentioning

confidence: 92%

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

Corazziari¹,

Pozzessere²,

Dani³

et al. 1978

Gut

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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...

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Effect of continuous infusion of pentagastrin on lower esophageal sphincter pressure and gastric acid secretion in normal subjects.

Cited by 25 publications

References 14 publications

Is gastrin a major determinant of basal lower esophageal sphincter pressure? A double-blind controlled study using high titer gastrin antiserum.

Is gastrin a major determinant of basal lower esophageal sphincter pressure? A double-blind controlled study using high titer gastrin antiserum.

Responses of the competent and incompetent lower oesophageal sphincter to pentagastrin and abdominal compression.

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

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