Plasma Gastrin and Gastric Acid Responses to Sham Feeding and Feeding in Dogs

Nilsson, Göran; Simon, Jonathan; Yalow, Rosalyn S.; Berson, Solomon A.

doi:10.1016/s0016-5085(19)33348-7

Cited by 135 publications

(38 citation statements)

References 21 publications

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“…These findings are very different from shamfeeding experiments in dogs (Nilsson et al, 1972), where atropine was found to block the rise in gastrin. While species difference may account for this, a further possible explanation is that the vagus contains fibres both to enhance and inhibit gastrin release.…”

Section: Discussioncontrasting

confidence: 95%

“…Sham-feeding causes release of gastrin in man (Mayer et al, 1974) and animals (Nilsson et al, 1972) but the mechanism is unclear. In dogs a gastrin-releasing mechanism under cholinergic control (Csendes et al, 1972;Nilsson et al, 1972) has been demonstrated. In humans, however, most workers show raised plasma gastrin after vagotomy Jaffe et al, 1974), implying impaired inhibition of release.…”

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confidence: 99%

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Role of neural influences in the release of gastrin, glucagon, and secretin during hypoglycaemia in man.

McLoughlin¹,

Hayes²,

Buchanan³

et al. 1978

Gut

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BelfastSUMMARY Both vagal and sympathetic innervation been have described as influencing hormone release from the gastrointestinal tract and pancreas. The role of neural influences on the release of gastrin, glucagon, and secretin has been studied using the potent autonomic nerve stimulus of hypoglycaemia. Healthy subjects were each rendered hypoglycaemic by insulin 0-2 units/kg on three occasions: after atropine 20 pg/kg: after propranolol 160 mg orally, and without prior drug administration.Adequate beta-blockade was confirmed by observation of the pulse rate response to a standard exercise at the end of the experiment, and by measurement of plasma propranolol levels. Hypoglycaemia failed to produce a rise in plasma gastrin under either propranolol or control conditions but a significant rise was noted with prior atropinisation. The glucagon response to hypoglycaemia, when measured with either the C-or N-terminal reactive antibodies, was found not to be influenced to any significant extent by either beta-blockade or atropinisation. No alteration in plasma secretin levels was noted during hypoglycaemia. It therefore appears that neural influences are relatively unimportant in the release of gastrin, glucagon, and secretin in man.

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Section: Discussioncontrasting

confidence: 95%

mentioning

confidence: 99%

Role of neural influences in the release of gastrin, glucagon, and secretin during hypoglycaemia in man.

McLoughlin¹,

Hayes²,

Buchanan³

et al. 1978

Gut

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“…They found that insulin hypoglycemia was accompanied by an increased rate of gastric secretion and a significant rise in gastrin levels in portal blood. In dogs with a gastric fistula and a vagally-innervated fundic pouch, sham feeding caused increases in serum gastrin concentration, accompanied by acid re sponses from the fundic pouch (81). With the gastric fistula closed, and thereby allowing full acidification of the antral mucosa, the rise in serum gastrin level was of relatively short duration.…”

Section: Control Of Gastrin Secretionmentioning

confidence: 99%

Secretion of Gastrointestinal Hormones

Andersson¹

1973

Annu. Rev. Physiol.

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Compared with development in other fields of hormone research, one must describe advances in the knowledge of gastrointestinal hormones as stumbling. The first evidence suggesting the existence of hormones in the mu cosa of the gastrointestinal tract was provided by Bayliss & Starling-for se cretin in 1902 (13), and by Edkins-for gastrin in 1905 (25). Apart from occasional important discoveries, gastrointestinal hormone research was then more or less dormant for almost 50 years. During this time there was much controversy as to whether the postulated hormones really existed; in fact, this debate continued until the hormones had been chemically identified and their specific biological actions subsequently demonstrated.As a result of the participation of research workers from several different branches of medical science, a considerable amount of new information on gastrointestinal hormones has accumulated during the last ten years, and this has acted as a strong stimulus to further research in this area. Morphologists have provided evidence on particular cells in the mucosa of the gastrointesti nal tract that might harbor various hormonal substances. Biochemists have succeeded in identifying, determining the structures of, and synthesizing the three "old" hormones, gastrin, secretin, and cholecystokinin-pancreozymin. Access to pure hormonal substances has made it possible for immunologists to work out sensitive and specific radioimmunoassays whereby the hormones can be detected and measured in tissues and body fluids. WHAT ARE THE CRITERIA FOR A GASTROINTESTINAL HORMONE?In recent years the number of possible candidates for new hormones has increased considerably. Evidence for a new gastrointestinal hormone has been based either on purely physiological observations or on the chemical isolation of a new agent from the gastrointestinal tract. It is therefore particu larly important for the following discussion to decide criteria that must be fulfilled before an agent can be classified as a gastrointestinal hormone. By definition, a hormone is a discrete chemical substance secreted by a specific tissue and transported to a distant site where it exerts its effect upon other specific tissues. Thus, in order to prove the existence of a gastrointestinal hor mone by physiological means one must show that the application of a physio-431 Annu. Rev. Physiol. 1973.35:431-452. Downloaded from www.annualreviews.org Access provided by Michigan State University Library on 02/03/15. For personal use only.Quick links to online content Further ANNUAL REVIEWS

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“…Nilsson et al (1) have shown that within 2 min after sham feeding commenced, circulating gastrin levels rose significantly. However, they did not determine a rate constant nor did they measure t w .…”

mentioning

confidence: 99%

“…Recently Nilsson et al (1) reported that endogeneous gastrin is released rapidly into the circulation in response to sham feedings; however, while sham feeding they do not describe in detail the hormone's rate of release.…”

mentioning

confidence: 99%

Kinetics of Gastrin Release and Degradation in Response to Electrical Vagal Stimulation in the Dog

Lanciault

Bonoma

Karreman

et al. 1973

Experimental Biology and Medicine

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The release and degradation of endogenous gastrin was studied using electrical vagal stimulation in the anesthetized dog. A mathematical model was developed to describe the rates of release and degradation of the gastrin hormone.Recently Nilsson et al.(1) reported that endogeneous gastrin is released rapidly into the circulation in response to sham feedings; however, while sham feeding they do not describe in detail the hormone's rate of release.The rate of degradation of endogenous circulating gastrin (as well as for the heptadeca-, penta-and tetrapeptide of the hormone) has been studied and was also found to be rapid (2-7). However, the conditions under which the studies were carried out were not appropriate for detailed measurement.Materials and Methods. Female mongrel dogs weighing 15-25 kg were fasted at least 18 hr prior to receiving 2 mg/kg morphine sulfate subcutaneously. Thirty minutes after receiving the morphine, the dogs were anesthetized with 100 mg/kg chloralose intravenously. A catheter was placed into the portal vein for sampling blood. The pyloric end of the stomach was ligated and an acute gastric fistula was made in the most dependent portion of the stomach. Gastric secretions were collected under vacuum. The cervical vagi were isolated bilaterally and the distal cut ends placed on platinum electrodes. The vagi were stimulated using 7 V, 10-15 Hz and 5 msec duration as the stimulus parameters (8). After a 60-min control period in which blood samples (5 ml vol) were taken at 15-min intervals, the vagi were continuously stimulated for 30 min. With the onset of the stimulus, blood samples were taken from the portal vein at 2.5-niin intervals for the entire period of stimulation. At the end of this period of stimulation, blood samples were taken every 2.5 min for the first 15 min; then a t 5-min intervals for the next 15 min; and finally every 15 min for the next 30 min. The blood was allowed to clot and the serum was stored at -20' until assayed.Gastric acid concentration (mEq/liter ) and output were determined electrometrically by titrating the gastric juice with 0.1 N sodium hydroxide to an endpoint of pH 7.0. Serum gastrin concentrations were determined by the double-antibody radioimmunoassay method of McGuigan (9).Results. Figure 1 shows the changes in circulating serum gastrin levels in response to electrical vagal stimulation. Basal gastrin levels prior to stimulation were 55-71 pg/ml with a mean of 62 t 3 (SEM) pg/ml.Electrical stimulation of the vagus produced a rapid and statistically significant rise in circulating serum gastrin concentrations within 2.5 min of onset of stimulation ( p < 0.05).Average concentrations between 150 and 175 pg/ml were noted during this early period of stimulation. The levels of gastrin remained constant for the next 10 min. At that time gastrin levels appeared to increase further but the rise was not statistically significant

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Plasma Gastrin and Gastric Acid Responses to Sham Feeding and Feeding in Dogs

Cited by 135 publications

References 21 publications

Role of neural influences in the release of gastrin, glucagon, and secretin during hypoglycaemia in man.

Role of neural influences in the release of gastrin, glucagon, and secretin during hypoglycaemia in man.

Secretion of Gastrointestinal Hormones

Kinetics of Gastrin Release and Degradation in Response to Electrical Vagal Stimulation in the Dog

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