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Biomedical subjects

H Koop

Publications and source records attributed to H Koop.

At least 91 records · Page 5Linked to original sources
PubMed1988

Somatostatin-gastrin interactions in the rat stomach.

Low concentrations of somatostatin and gastrin within or slightly above the range of physiologically circulating levels were perfused in the isolated, vascularly perfused rat stomach preparation. Somatostatin at 10 and 50 pg/ml significantly inhibited acetylcholine-stimulated gastrin secretion by 26% and 45%, respectively, whereas perfusion of 50 and 500 pg/ml exogenous gastrin did not modify gastric somatostatin secretion. Perfusion of somatostatin-antiserum significantly increased gastrin release by 235%. It is concluded that (1) somatostatin is a powerful inhibitor of the gastrin cell under in vitro conditions; the data are in accordance with a concept that endogenous somatostatin could act as a true hormone; (2) the secretory activity of the somatostatin cell is not significantly affected by circulating gastrin.

Acetylcholine↗
PubMed1988

Effect of cholestyramine on plasma cholecystokinin and pancreatic polypeptide levels, and exocrine pancreatic secretion.

The effect of acute and long-term administration of cholestyramine, a non-absorbable bile salt binding resin, on exocrine pancreatic secretion, plasma-cholecystokinin (CCK) and plasma-pancreatic polypeptide (PP) was investigated in 10 healthy volunteers. Oral ingestion of 12 g cholestyramine augmented the stimulatory effect of a liquid test meal on plasma-CCK (3.5-fold) and plasma-PP (2-fold). During prolonged treatment with 3 x 12 g cholestyramine daily for 4 weeks, the most pronounced increase in basal hormone levels was observed after 1 day, but progressively decreased during treatment and had normalized after 4 weeks. However, the stimulated plasma-CCK output was still significantly elevated after cessation of treatment, compared with pretreatment values. After acute and chronic cholestyramine administration only stimulated lipase secretion was elevated, whereas trypsin and amylase remained unchanged. It is suggested that removal of bile salts enhances CCK and thereby PP release and pancreatic lipase secretion.

Adult↗
PubMed1988

Influence of prolonged antacid administration on rat gastric mucosa.

The effect of long-term administration of an antacid preparation on the gastric mucosa was investigated in rats, special attention was directed towards hypergastrinaemia and density of argyrophil cells. One ml of an Al (OH)3- and Mg (OH)2-containing antacid (in vitro neutralization capacity 28 mmol/die) or water was administered intragastrically 4 times daily. An additional group of rats remained untreated. Twelve hours after the final dose serum gastrin levels were significantly (p less than 0.001) elevated (113 +/- 28 pg/ml) compared to the control groups (33 +/- 1 and 22 +/- 2 pg/ml). Antral gastrin (G)-cell density was also increased after antacids by 58% whereas the somatostatin (D)-cell density and the somatostatin concentration in antral tissues were decreased. The number of fundic D- and argyrophil cells were not altered by antacid treatment. The number of parietal cell declined significantly in response to antacids. The foveolar gland region was almost doubled after antacids. It is concluded that in the rat 1. despite persistent hypergastrinaemia due to chronic antacid administration increases in argyrophil cell densities are not to be found; 2. long-term administration of antacids exert a trophic effect on the corpus mucosa predominantly by an increase of mucus neck cells.

Aluminum Hydroxide↗
PubMed1988

[Reduced suppression of gastric acid by ranitidine in severe reflux esophagitis. A pilot study].

Repeated intragastric long-term pH recordings for 24 h were conducted in 13 patients with reflux oesophagitis grade III and IV (Savary and Miller) during treatment with ranitidine 150 mg b.i.d. and 300 mg b.i.d. and omeprazole 40 mg mane (n = 5). Ranitidine led to a significantly less pronounced increase in median gastric pH in oesophagitis than in healthy controls. The magnitude of intragastric pH increase showed parallelism to symptomatic response and healing. Omeprazole increased intragastric pH above 4 for 24 h and caused rapid healing in non-responders. It is concluded that in patients with severe reflux oesophagitis ranitidine is less effective in increasing intragastric pH than in controls, whereas omeprazole reveals potent antisecretory activity accompanied by rapid healing.

Adult↗
PubMed1987

Influence of chronic omeprazole treatment on gastric endocrine function.

The influence of a 4-week treatment with the substituted benzimidazole omeprazole (20 mg daily) or placebo on gastric endocrine function was tested in healthy male volunteers. Compared with placebo-treated subjects basal serum gastrin levels were slightly but significantly increased after treatment with omeprazole from 10 to 22 pg/ml (medians; P less than 0.05) but returned to pretreatment values after 2 weeks recovery (9 pg/ml). Antral gastrin tissue concentration increased and was still elevated after recovery; however, antral gastrin concentrations also increased in placebo controls, and increments immediately after cessation of omeprazole treatment (2.58 micrograms/g; median) were not significantly over control values (1.92 micrograms/g; P greater than 0.1). Postprandial gastrin release, basal and food-stimulated insulin release, antral somatostatin concentration, and volume densities of antral G and D cells were unaffected. It is concluded that, due to incomplete inhibition of gastric acid secretion at the omeprazole dose studied, only slight effects on the endocrine stomach are to be expected after 4 weeks of administration of omeprazole.

Adult↗
PubMed1987

Calcitonin gene-related peptide stimulates rat gastric somatostatin release in vitro.

The influence of rat calcitonin gene-related peptide (rCGRP) on the secretion of gastric somatostatin and gastrin was studied in vitro using the isolated, vascularly perfused rat stomach preparation. rCGRP stimulated somatostatin secretion dose-dependently reaching 3-fold stimulation at 1 microM. The kinetics of somatostatin response were characterized by a sharp increase in the initial phase of rCGRP perfusion followed by sustained elevated levels. Gastrin secretion was moderately suppressed at 1 nM to 100 nM CGRP. Somatostatin responses to half-maximal stimulation with 100 nM CGRP were not affected by concomitant perfusion of atropine, propranolol, and tetrodotoxin. It is concluded that increases in somatostatin release in response to CGRP are probably due to a direct effect on the gastric somatostatin-producing D-cell and may be important for the potent acid-inhibitory activity of CGRP.

Animals↗
PubMed1987

Influence of chronic drug-induced achlorhydria by substituted benzimidazoles on the endocrine stomach in rats.

The release of gastric somatostatinlike immunoreactivity and gastrin was studied in rats with chronic achlorhydria induced by the substituted benzimidazole BY 308. In vitro, stimulation of gastrin release by acetylcholine was slightly enhanced after 1 day of treatment but no further effects were observed compared to placebo controls. Four weeks of treatment evoked marked gastrin hypersecretion, which was atropine-resistant. Stimulation of gastrin release was inversely correlated to enhancement of basal gastrin levels. Chronic achlorhydria distinctly reduced somatostatin responses to isoproterenol, whereas potent stimulation was observed in controls. Treatment with BY 308 for 1 wk was associated with fully developed gastrin hypersecretion but isoproterenol-stimulated somatostatin release was still unaffected. Hypergastrinemia accompanied by increased antral gastrin and reduced antral and fundic somatostatin concentrations was also found in vivo after 4 wk of treatment with BY 308. It is concluded that chronic achlorhydria not only enhances storage and secretion of gastrin but also diminishes the secretion and tissue stores of somatostatin; adaptive changes of the somatostatin cell occur, however, with a much longer delay.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed1987

Increased visualization of antral gastrin-producing G-cells after acute stimulation of gastrin release in the rat.

The effect of acute stimulation of gastrin release on the number of antral gastrin-producing G-cells stained by conventional immunohistology was investigated in two experimental models. The substituted benzimidazole derivate BY 308 was administered at a dosage that induces complete achlorhydria and thereby led to marked hypergastrinaemia. Two hours after drug administration, antral G-cell density was increased by 14% and 35% in 12-h and 48-h fasted rats, respectively. Both serum gastrin levels and G-cell density further increased after 3 and 8 days' treatment with BY 308 whereas the somatostatin (D)-cell count did not change prior to 8 days' administration. In the isolated, vascularly perfused rat stomach, acetylcholine was perfused for 36 min; this regimen increased gastrin release four-fold and enhanced the G-cell count by 24% whereas 8 min acetylcholine perfusion did not alter G-cell density significantly but stimulated gastrin output. The results of this study suggest that acute changes in the secretory activity of the gastrin cell are accompanied by an alteration of the staining characteristics thus indicating that an increase in the antral G-cell count does not solely depend upon formation of new cells.

Acetylcholine↗
PubMed1987

Effect of food deprivation on the function of the intestinal cholecystokinin-producing cell in the rat.

The influence of fasting and refeeding on storage and secretion of cholecystokinin (CCK) was investigated in the rat. Groups of rats deprived of food for 12 and 96 h were studied. Animals of each group received 0.75 g of long-chain triglycerides or water via an orogastric tube after the fasting period 15 min prior to exsanguination. Rats fed ad libitum served as controls. Duodenal, jejunal and ileal segments were dissected for tissue extraction and immunohistochemical staining of CCK-containing cells. Fasting over 96 h resulted in a significant reduction of plasma CCK, duodenal CCK concentrations and number of duodenal CCK-containing cells. Changes were less pronounced in the more distal parts of the small bowel. Refeeding caused an increase in plasma and tissue CCK concentrations, thus abolishing all significant differences that occurred during fasting. Gel chromatography of tissue extracts showed a shift towards the bigger molecular forms after 96 h of fasting. We conclude that storage and secretion of gut CCK are reduced during food deprivation in rats. The reduction of tissue CCK appeared at the expense of the lower molecular forms. However, the functional responsiveness of the CCK cell as indicated by the postprandial rise in plasma CCK seems to be maintained after a 4-day fast.

Animals↗
PubMed1987

[Gastrin in the pathogenesis of ulcer disease].

The role of endogenous gastrin in the pathogenesis of "idiopathic" ulcer disease is difficult to determine; however, gastrin is probably only of limited importance besides various probable more important factors. In conditions associated with uncontrolled gastrin production by a gastrin secreting tumor or in cases in which the feedback regulation between gastrin release and intragastric pH is disturbed severe and recurrent ulcers may develop. Radioimmunological determination of serum gastrin levels enable to identify such cases of ulcer disease due to an excess of circulating gastrin.

Gastric Acid↗
PubMed1986

Hormonal and cardiovascular variations during a public lecture.

A long-time electrocardiogram over a period of 12 h was recorded from ten test persons without cardiovascular diseases, and their blood pressure was checked at regular intervals on the day of a public speech. In order to determine plasma concentrations of epinephrine, norepinephrine, cortisol, human growth hormone (hGH), prolactin and gastrin, blood samples were taken from the subjects by inserting a venous catheter in the morning. The levels of epinephrine, norepinephrine and cortisol were also examined in urine collected from the volunteers. During the public speech there was a distinct increase in blood pressure and pulse rate. Epinephrine and cortisol showed the clearest increase in serum and collected urine, whereas norepinephrine, prolactin, hGH and gastrin reacted less strongly. The epinephrine/norepinephrine ratio value is discussed as a parameter for psychomental and emotional strain.

Adult↗
PubMed1986

Effect of starvation on endocrine cells in the rat stomach.

The influence of food deprivation on gastric G- and D-cells and on parietal cells was studied in the rat. In fed controls and groups of rats fasted for 12 and 96 h G-, D- and parietal cell densities, somatostatin and gastrin concentration in antral and fundic specimens and serum gastrin were compared. Gastrin in antral mucosa, serum gastrin, G-cell density as well as antral D-cell density decreased in long-term fasted rats by 52%, 90%, 58% and 42%, respectively. Fundic D-cell density remained unchanged. After 96 h starvation somatostatin concentration slightly increased in antral mucosa (+35%; P less than 0.05), but decreased in fundic mucosa (-40%; P less than 0.05). Parietal cell density was not influenced by prolonged fasting. These findings demonstrate that changes in D-cell morphology and mucosal somatostatin content are not parallel and that the rat gastric D-cell is less dependent on food in the gastric lumen than the G-cell. The unaltered fundic D-cell density reflects the functional activity of gastric D-cell which has also been shown to be independent of the presence or absence of food.

Animals↗
PubMed1986

Control of rat gastric somatostatin release by gamma-aminobutyric acid (GABA).

The influence of gamma-aminobutyric acid (GABA) on gastric somatostatin and gastrin release was studied using an isolated perfused rat stomach preparation. GABA dose-dependently inhibited somatostatin release (maximal inhibition of 44% at 10(-5)M GABA), whereas gastrin secretion was not affected. The GABA agonist muscimol led to a decrease in somatostatin release of similar magnitude. The GABA-induced changes were partially reversed by 10(-5)M atropine. Gastrin secretion was not influenced by either protocol. It is concluded that GABA as a putative neurotransmitter in the enteric nervous system is inhibitory to rat gastric somatostatin release in vitro via cholinergic pathways.

Animals↗
PubMed1986

Trophic effect of truncal vagotomy on the rat pancreas.

The trophic effect of truncal vagotomy was studied in rats. Three months after vagotomy and pyloroplasty pancreatic weight was significantly increased by 40% (p less than 0.001). Gastric stasis and consecutive distension of the stomach was observed in the majority of vagotomized animals despite pyloroplasty; the trophic effect of vagotomy on the pancreas was most pronounced in animals with severe stomach distension. Basal gastrin levels were increased after truncal vagotomy but did not correlate to gastric stasis and to the hypertrophy and hyperplasia of the exocrine pancreas. Basal pancreatic polypeptide hexapeptide levels were not altered after vagotomy. Morphometric studies on the endocrine pancreatic tissue showed that the relative volume density decreased due to the increase in exocrine tissue. However, the total islet cell mass remained constant. It is concluded that chronic truncal vagotomy has a trophic effect on the exocrine but not on the endocrine pancreas; additional factors besides gastrin seem to be responsible for this.

Animals↗