Proceedings: Measurement of gastric mucosal potential difference at endoscopy.
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Biomedical subjects
Publications and source records attributed to D G Colin-Jones.
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The absorption of (14)C-labelled glyceryl tripalmitate was tested in 62 patients by determining the maximum specific activity of CO(2) in the breath after an oral dose. A significant correlation with faecal fat excretion was found. The absorption of (14)C labelled palmitic acid was tested subsequently in 54 patients. In cases of pancreatic steatorrhoea, normal absorption of palmitic acid with impaired absorption of glyceryl tripalmitate was found, whereas in most patients with coeliac disease the absorption of both substances was depressed to the same extent.
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A mentally subnormal patient presenting with oedema was found at gastroscopy to have a large trichobezoar and multiple gastric polyps. The serum concentrations of albumin and IgG were low in the absence of proteinuria, and the gastrointestinal clearance of radiochromium after the intravenous administration of radiochromic chloride was increased. These findings are compatible with increased gastrointestinal loss of plasma proteins. In addition, the patient had steatorrhoea. All of these abnormal findings were markedly improved after operative removal of the bezoar.
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A perfused rat stomach technique which can detect synthetic human gastrin I in amounts greater than 10 ng and measure by block assay amounts greater than 50 ng was used to study circulating gastrin-like activity in normal subjects, patients with peptic ulcer, and patients with the Zollinger-Ellison syndrome. No detectable activity was found in normal subjects or patients with gastric ulcer before or after meals. No activity was found in the fasting plasma of patients with duodenal ulcer but after meals activity could be detected in duplicate samples in seven of 20 patients. In nine proven cases of the Zollinger-Ellison syndrome, gastrin-like activity in the plasma ranged from 15 to 356 ng/ml. The gastrin-like content of two tumours was 6.4 and 29.1 mug/g of tissue. The significance of these findings in relation to immunoassay is described.
1. The injection of 2-deoxy-D-glucose directly into the lateral hypothalamic area of rats, but not elsewhere, caused a prompt and sustained secretion of acid by the stomach at a rate comparable to that due to insulin hypoglycaemia.2. Acid secretion provoked by such injections, like that resulting from hypoglycaemia, could be stopped by raising the plasma glucose concentration by the intravenous infusion of glucose.3. Unilateral intrahypothalamic injection of 2-deoxy-D-glucose activated both vagi for, although cutting one vagus reduced the secretion, division of both was necessary to abolish it.4. Gastric acid secretion evoked by a systemic stimulus (insulin-induced hypoglycaemia or intravenous 3-O-methylglucose) could be prevented by inactivating the lateral hypothalamic area on each side with phenol or lignocaine.5. It is concluded that there exists in the lateral hypothalamic area a chemoreceptor, responsive to a lack of metabolizable glucose, which can initiate and sustain the vagally mediated secretion of acid by the stomach.
1. A method is described for the bio-assay of gastric secretagogues using the perfused rat stomach in which the acid output can be readily and accurately quantified.2. This technique increases the sensitivity of the perfused rat stomach so that 10-20 ng of synthetic human gastrin I can be detected.3. It is possible to assay secretagogues, relative to a standard with fiducial limits of less than +/-30%.4. The use of this system is illustrated by assays comparing synthetic human gastrin I with pentagastrin, pure hog gastrin and gastrin added to plasma.
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1. The onset of the secretion of acid from the stomach of rats during insulin-induced hypoglycaemia has been found to correspond to a mean plasma glucose concentration of 72 mg/100 ml. (equivalent to a blood glucose concentration of 44 mg/100 ml.).2. Infusions of the non-metabolizable sugar, 3-O-methylglucose, into rats with denervated adrenal glands caused a large and sustained rise in the gastric acid output. This gastric acid secretion could be prevented by prior vagotomy or stopped, when previously established, by cutting the vagi or by the administration of glucose.3. A consistent relationship was demonstrated between the plasma concentration of glucose and the total concentration of glucoses (glucose plus 3-O-methylglucose) in the plasma at the onset of gastric acid secretion during the infusion of 3-O-methylglucose into these rats. The theoretical basis for this relationship is discussed.4. 3-O-methylglucose did not cause the release of gastric acid when infused into rats with intact sympathetic nervous systems owing to the effects of the secretion of adrenaline provoked by this agent.5. The qualitative and quantitative similarities between the factors governing both the secretion of gastric acid and the release of adrenaline in the absence of a sufficiency of metabolizable glucose are discussed. It is suggested that the reactions of both these systems under such circumstances are determined by chemoreceptors which possess identical characteristics.
The physiological factors which determine the penetration of the brain by 2-deoxy-D-glucose have been studied and the practical importance of the blood-brain barrier has been demonstrated. The evaluation of the gastric secretory response to 2-deoxy-D-glucose has been shown to depend upon the plasma glucose concentration. It is concluded that because of the hazards and uncertainties in the use of 2-deoxy-D-glucose in man its use is to be deprecated.
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The availability of highly effective ulcer-healing agents has made drug therapy the treatment of choice for the large majority of patients with peptic ulceration. Attention has now shifted from healing to reduction of the very high relapse rates still seen with most drug regimens.
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