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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effect of adrenergic blockade on gastric secretion altered by catecholamines was studied for 4 hr after injection in rats with chronic gastric fistulas. The alpha-adrenergic blockers phenoxybenzamine and phentolamine significantly inhibited the basal secretion of HCl and pepsin. Blockade of the beta-adrenergic receptors with propranolol did not change this secretion. Practolol in small doses slightly increased and in larger doses inhibited HCl out-put. Of the catecholamines, adrenaline and dopamine most markedly reduced HCl and pepsin secretion, while noradrenaline and isoprenaline had a weaker effect. Neither alpha- nor beta-adrenergic blockers prevented the inhibitory action of the catecholamines employed, but intensified the depression of the gastric secretion provoked by them. Adrenergic blockers inhibited secretion after catecholamines as well as basal secretion. This indicates that these two antagonistic groups of compounds act independently on the mechanism controlling gastric secretion. It is unlikely that this takes place indirectly through changes in the blood supply of the gastric mucosa.
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PMID:Effect of adrenergic blockade on gastric secretion altered by catecholamines in rats. 1 61

Insulin was adsorbed to a strongly acidic ion exchanger and incubated with pepsin. The digestion of the matrix-bound insulin was found to be restricted to the cleavage of the peptide bond between phenylalanine-B25 and tyrosine-B26. Factionation of the reaction products was achieved by gel filtrationon Sephadex G-50 at pH 8 where des-pentapeptide(B26-30)-insulin does not aggregate. Another way to purify this compound was ion-exchange chromatography, which was easy due to the loss of one positive charge on the modified insulin. Crystallization could be achieved in a phenol-containing buffer. Des-pentapeptide(B26-30)-insulin was found to be molecularly uniform by electrophoresis at pH 2.2 and 8.6, thin-layer chromatography, performic acid oxidation, end group analysis and amino acid analysis. The CD-spectrum indicated conformational changes compared to insulin. The biological activity was considerably reduced: fat cell assay 20%, blood sugar depression 30%.
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PMID:[B-chain shortening of matrix-bound insulin by pepsin, I:Preparation and properties of bovine des-pentapeptide(B26-30) insulin (suthor's transl)]. 24 Jul 71

VIP and secretin were compared in regard to their effects on gastric acid and pepsin secretion induced by pentagastrin histamine or a peptone meal as well as on gastric mucosal blood flow and meal induced serum gastrin level in conscious dogs provided with gastric fistulas and denervated fundic pouches. Both VIP and secretin caused a dose-related stimulation of basal pepsin outputs and inhibition of pentagastrin-induced acid secretion. VIP, like secretin, inhibited pentagastrin and meal-induced gastric acid secretion but in contrast to secretin it caused inhibition of acid response to histamine. Inhibition of acid secretion by VIP or secretin was accompanied by secondary reduction in gastric mucosal blood flow in tests with pentagastrin or histamine and by depression of the serum gastrin level in tests with a peptone meal. This study indicates that in comparison with secretin, VIP has a wider spectrum of inhibition of stimulated gastric secretion and may be considered as one of the enterogastrones released in the small intestine.
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PMID:Comparison of vasoactive intestinal peptide (VIP) and secretin in gastric secretion and mucosal blood flow. 76 58

Isoproterenol infusions depress pentagastrin (PG)-stimulated secretion of acid and pepsin from both gastric fistulae and denervated (Heidenhain) pouches in conscious dogs. It was not found to do so if methacholine replaced gastrin. Propranolol reversed the isoproterenol depression of PG stimulation but had no effect on isoproterenol plus methacholine except on the fistula where both acid and pepsin were depressed. It is felt that PG and methacholine act by differing mechanisms both on chief and parietal cells.
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PMID:Adrenergic activity and gastric secretion. 77 88

The effect of various doses of serotonin (5-HT) on the basal or insulin-stimulated gastric secretion was studied, for 4 hr after the injection, in unanesthetized rats with chronic gastric fistulas. The blood glucose and serum Na, K and Ca ions concentrations were also determined. Insulin produced hypoglycemia and hypokalemia, most pronounced in the first hr, and increased HCl and pepsin output, with a maximum at 2 hr after the injection. 5-HT significantly inhibited both basal and insulin-stimulated gastric secretion. The amine produced transient hyperglycemia, which was less pronounced in rats simultaneously receiving insulin. The inhibition of insulin-stimulated gastric secretion by 5-HT lasted for a longer period than the prevention of the biochemical changes brought about by insulin. The prevention by 5-HT of insulin hypoglycemia and hypokalemia may be of significant importance in the mechanism of the depression of insulin-stimulated gastric secretion.
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PMID:The influence of serotonin on insulin-stimulated gastric secretion, blood glucose and serum electrolyte levels in the unanesthetized rat. 116 2

It would seem that a gastric ulcer is the product of an interaction between chronic gastritis, the acid (and pepsin) of the gastric juice, and one or more precipitating factors. In a group of 194 consecutive patients with gastric ulceration particular note was made of whether they smoked, drank alcohol, used salicylates, were depressed or had experienced recent stress. There was an extraordinarily high incidence of depression among White women.
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PMID:Alcohol, aspirin, depression, smoking, stress and the patient with a gastric ulcer. 126 62

Intragastric administration of a synthetic analog of prostaglandin E2 to patients with duodenal ulcers results in depression of the gastric acid production and in reduction of potassium level, leads to an elevation of the sialic acid debit and a rise of sodium concentration, not essentially changing calcium, chlorides, and pepsin levels. A combined analysis of gastric acid production and measurements of sialic acids, sodium and potassium detect the imbalance of the mucoid and bicarbonate secretion in peptic ulcers, this helping predict the disease course.
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PMID:[The cytoprotective effect of prostaglandin E2 in duodenal ulcers]. 247 1

The effects of different thermal processes used to produce ready-to-eat cereals on the glycemic response to whole grain wheat were investigated in rats. The metabolic response to drum dried flour, which constitutes the major component in instant gruel and porridge, was also studied in healthy human subjects. Boiled flour was used for comparison. The degree of starch gelatinization and rate of starch hydrolysis in vitro were also measured. Incompletely gelatinized steam flaked and dry autoclaved products were digested more slowly in vitro and elicited lower glucose responses in rats compared with completely gelatinized drum dried, extrusion cooked or boiled samples. The initial glycemic response in rats was closely related to the rate of starch hydrolysis in the pepsin/alpha-amylase assay (r = 0.91, P less than 0.04). When pepsin was omitted, no significant correlation was obtained. The peak glucose, insulin and C-peptide responses in humans after breakfast meals of porridge prepared from drum dried flour and from boiled flour were similar, whereas the rate of depression of the glucose curve was more rapid after consuming drum dried porridge. It is concluded that the glycemic response to wheat products is affected by the processing conditions used. The more severe the processing conditions, the more rapid the digestion of starch.
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PMID:The effect of various thermal processes on the glycemic response to whole grain wheat products in humans and rats. 268 9

The evidence that duodenal ulcer is a psychosomatic disorder is reviewed. A variety of both experimental stressors and differing states of emotional arousal (anxiety and anger in particular) are associated with increased acid and pepsin secretion. Furthermore, chronic life stressors predispose to duodenal ulcer, presumably by way of symptomatic anxiety or depression, while poor social support may comprise another risk factor. Subjects with high levels of trait anxiety or neuroticism are more prone to stress-induced anxiety and its physiological consequences. There is minimal acceptable evidence to support more specific personality-related theories, including Type A behaviour, alexithymia or the earlier psycho-analytic theories of Alexander. Nonetheless, it is concluded that Alexander's inclusion of duodenal ulcer as one of a handful of classic psychosomatic disorders has been confirmed. Since some 40% of duodenal ulcer patients relapse in the first year after medical treatment, there may be some role for psychological treatments (especially in the domain of stress/anxiety management) for those patients who relapse and have co-existing high state or trait anxiety or exposure to chronic stressors.
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PMID:Psychosocial causes of duodenal ulcer. 304 60

In unanesthetized dogs with Heidenhain pouches and separated duodenal pouches, intravenous infusion of commercial cholecystokinin (1.0 IDU per min) produced a significant depression of pouch acid and pepsin secretion stimulated by pentagastrin (1.0 microg per min) or by methacholine (2.0 microg per min). Acid response to methacholine was temporarily augmented. Irrigation of the duodenal pouches with emulsified fat produced similar patterns of depression of acid secretion in response to pentagastrin and pepsin secretion in response to pentagastrin or methacholine. Acid secretion stimulated by methacholine was temporarily augmented after the irrigation. It is concluded that fat releases endogenous cholecystokinin from the duodenal mucosa and that cholecystokinin, or duodenal fat, powerfully depresses Heidenhain pouch pepsin secretion in dogs. The involvment of the gastric inhibitory polypeptide (GIP) cannot be assessed from the present experiments.
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PMID:Inhibition of Heidenhain pouch pepsin secretion by commercial cholecystokinin and duodenal fat in dogs. 460 62


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