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Biomedical subjects

H Koop

Publications and source records attributed to H Koop.

At least 109 records · Page 6Linked to original sources
PubMed1986

Effect of the prokinetic drug cisapride on gastrointestinal hormone release.

The influence of the prokinetic drug cisapride on the release of gastrointestinal hormones was studied in volunteers. First, acute effects of single doses of cisapride compared with saline were investigated. Cisapride at doses of 8 mg and 20 mg intravenously significantly increased plasma concentrations of pancreatic polypeptide (hPP) by 145% and 146%, respectively. Cholecystokinin (CCK) levels were increased by 176% at 8 mg cisapride, whereas gastrin and insulin levels remained unchanged. Enhancement of PP and CCK secretion was almost completely abolished by pretreatment with 1 mg atropine. Carbachol (250 micrograms subcutaneously) increased PP release by 62% but did not affect the other hormones. Second, the influence of a 1-week treatment (10 mg three times daily, given orally) on plasma hormone levels was studied. After 1 week the postprandial CCK release was diminished by 58%. Basal levels and postprandial responses of gastrin, PP, and insulin were not altered by prolonged cisapride administration. It is concluded that acute application of cisapride stimulates secretion of PP and CCK via atropine-sensitive mechanisms and that chronic treatment with cisapride diminishes CCK release by an unknown mechanism.

Adult↗
PubMed1986

Effect of acid inhibition on gastric endocrine cells.

There is increasing evidence that the numbers of antral G cells and of fundic argyrophil (ECL) cells are influenced by agents that inhibit gastric acid secretion. Antral G cells increase in states of achlorhydria in man and animals provided atrophic antral gastritis is absent. In rats, treatment with substituted benzimidazoles like omeprazole and BY 308 increase G-cell densities dose-dependently. Even high doses of histamine H-2 antagonists and antacids increase antral G-cell densities. In contrast to G cells, antral D cells decrease in these instances. Fundic ECL cells increase in all experimental conditions of complete achlorhydria provided intact antral mucosa is present, i.e. there is elevated serum gastrin. Antacid treatment is not followed by an increase of fundic ECL cells, which could be explained by the less sustained increase of serum gastrin.

Animals↗
PubMed1986

Estimation of serum pancreatic isoamylase: its role in the diagnosis of exocrine pancreatic insufficiency.

Using an inhibitor method, fasting levels of pancreatic isoamylase were measured in 46 healthy controls and in 218 patients undergoing a secretin-pancreozymin test for diagnostic purposes, and compared with immunoreactive trypsin (IRT). Exocrine pancreatic insufficiency was found in 82 of the patients. The specificity of both enzymes was high in patients with nonpancreatic diseases (pancreatic isoamylase: 98.5%, IRT: 96.3%). No patient with nonpancreatogenic steatorrhea had a low serum enzyme value. Sensitivity was, unfortunately, low in patients with exocrine pancreatic insufficiency (pancreatic isoamylase: 45.1%, IRT: 41.5%) and increased only slightly when patients after an acute attack of the disease, or patients with pseudocysts or older than 60 were excluded (pancreatic isoamylase: 67.9%, IRT: 58.5%). Although highly specific, pancreatic isoamylase measurement is not sensitive enough to be used as a screening test for exocrine pancreatic insufficiency but may be used to determine the etiology of steatorrhea.

Cholecystokinin↗
PubMed1985

Role of endogenous prostaglandins in somatostatin-induced inhibition of gastrointestinal hormone secretion.

Endogenous prostaglandins have been reported to be essential for the inhibitory effect of somatostatin on acid secretion. From these results it could be suggested that the effect of somatostatin on the secretion of gastroentero-pancreatic hormones may also be medulated by prostaglandins. This hypothesis was investigated in man and in the rat. Somatostatin-induced inhibition of postprandial gastrin, cholecystokinin, pancreatic polypeptide, and insulin release was not influenced by indomethacin pretreatment in healthy subjects. Using the isolated perfused rat stomach preparation, inhibition of acetylcholine-stimulated gastrin secretion by somatostatin was found to be unchanged by indomethacin treatment. It is concluded that endogenous prostaglandins are unlikely to be indispensable for the inhibitory effect of somatostatin on gastroentero-pancreatic endocrine cells.

Adult↗
PubMed1984

Serotoninergic control of somatostatin and gastrin release from the isolated rat stomach.

The influence of exogenous serotonin on the secretion of gastric somatostatin and gastrin was investigated under in vitro conditions using an isolated, vascularly perfused rat stomach preparation. Serotonin stimulated gastrin release, maximal effects were observed at 10(-6) M which increased gastrin levels by 78%; on the contrary, somatostatin secretion was inhibited (maximal inhibition of 56% at 10(-6) M). Changes in hormone secretion in response to serotonin were reversed by combined blockade of 5-HT1 and 5-HT2 receptors by methysergide and blockade of 5-HT2 receptors by ketanserin (10(-5) and 10(-6) M, respectively), and of cholinoreceptors by atropine (10(-5) M). It is concluded that in rats in vitro serotonin inhibits release of gastric somatostatin and stimulates gastrin secretion via specific serotonin receptors but muscarinic cholinergic receptors are also involved.

Animals↗
PubMed1984

Pancreatic polypeptide and gastrin release during sham feeding in man.

During modified sham feeding (MSF) the role of endogenous gastric acid secretion and the influences of the autonomic nervous system on the release of pancreatic polypeptide (PP) and gastrin have been studied in 12 healthy subjects (aged 24-38 years). Sham feeding was performed without pretreatment (control) and after pretreatment with 400 mg cimetidine, 80 mg propranolol (both given orally) or 1 mg atropine administered subcutaneously 60 min prior to sham feeding. MSF induced a significant increase (about 100%) in PP release. Its early peak was reduced by pretreatment with propranolol whereas cimetidine had no effect. Atropine completely abolished the PP response. Gastrin release was stimulated by MSF only after prior administration of cimetidine and, to a lesser extent, after atropine pretreatment. It is concluded that: (1) the PP release after stimulation is under strong cholinergic control but is also mediated--particularly in the early phase--by adrenergic mechanisms; (2) endogenously released acid during vagal stimulation plays a minor role in the modulation of PP secretion, but (3) masks gastrin response to MSF.

Adult↗
PubMed1984

Effect of antacid and H2-receptor blocker treatment on gastric endocrine cells.

It has been previously suggested that antral pH governs the density of antral G- and D-cells. Therefore, we investigated the effect of acid neutralization by an antacid (magaldrat; in vivo neutralization capacity of 144 mval/day) and the effect of suppression of gastric acid secretion by an H2-receptor blocker (oxmetidine, 400 mg/day) on the density of both cell types in healthy volunteers and duodenal ulcer patients. Four weeks after antacid treatment antral G-cell density decreased significantly in both groups, while antral D-cells decreased only in volunteers. Basal serum gastrin was not altered, whereas the integrated postprandial serum gastrin response and antral gastrin concentration was significantly reduced in volunteers but not in ulcer patients. None of the parameters investigated was changed by oxmetidine treatment. Considering the short-lasting effect on acid neutralization induced by the antacid dosage used in this study and the inability of oxmetidine treatment to influence volume densities and secretory activities of antral G- and D-cells it is concluded that mechanisms other than a change of antral pH may account for the results obtained during antacid treatment.

Adult↗
PubMed1984

Pancreatic polypeptide response to sham feeding in man.

The relationship between gastric acid secretion and the release of pancreatic polypeptide (PP) during modified sham feeding was studied in 29 duodenal ulcer patients and 10 healthy controls. Ulcer patients showed higher basal plasma PP levels than age-matched controls (p less than 0.01). Acid secretion and PP levels were stimulated in the majority of patients and controls during sham feeding; however, no correlation was found between basal and vagally stimulated acid secretion and basal PP levels. Gastrin levels did not change in both groups. It is concluded from the present study that changes in plasma PP levels do not reflect sham feeding induced stimulation of the parietal cells.

Adult↗
PubMed1983

Pulmonary complications in fatal acute hemorrhagic pancreatitis.

Morphological changes of the lung occur frequently in fatal acute hemorrhagic pancreatitis. The pulmonary alterations are independent of mechanical ventilation and therefore not due to iatrogenic damage caused by high inspired oxygen concentrations. The histological findings are similar to those seen in the so-called shock lung syndrome. The pulmonary lesion develops progressively and three stages can be separated: early, late, and final phase. The pulmonary complications in acute hemorrhagic pancreatitis may be explained by the release of mediators such as pancreatic enzymes or free fatty acids into the blood stream. In acute hemorrhagic pancreatitis a close monitoring for shock parameters is necessary. A fall in arterial PO2 is an early indication for mechanical ventilation, including positive end-expiratory pressure.

Acute Disease↗
PubMed1983

Adrenergic control of rat gastric somatostatin and gastrin release.

The effect of adrenergic agonists and antagonists on the secretion of gastric somatostatin-like immunoreactivity (SLI) and gastrin was investigated in an isolated, vascularly perfused rat stomach preparation. Two- to six-fold increases in SLI secretion induced by isoproterenol, epinephrine, and norepinephrine were completely abolished by propranolol but were not influenced by phentolamine. Propranolol did not alter glucagon- and DB-cAMP-induced stimulation of SLI release. Experiments in which the beta 2-agonist salbutamol and the beta 1- and beta 2-blockers practolol and H35/25 were used showed that both subtypes of beta receptors are involved. Gastrin secretion revealed only minor changes in dose-response studies with a wide range of isoproterenol concentrations (2 X 10(-8) to 1.5 X 10(-4) M). The results obtained in this study suggest that in rats 1) the SLI response to adrenergic agonism is predominantly mediated by beta receptors; 2) both beta 1- and beta 2-adrenergic receptors are involved; 3) under in vitro conditions, adrenergic agonism is a weak stimulus for gastrin secretion.

Adrenergic beta-Agonists↗
PubMed1983

[Effect of drugs with acid-neutralizing and acid-suppressive effect on parietal cell function and on gastrin and somatostatin cell density of the stomach].

4 weeks treatment of healthy volunteers with Magaldrate (Al-Mg-containing antacid) is followed by an increase of basal serum gastrin, and a decrease of the antral G-cell density. Gastric acid secretion remained unchanged. In contrast, during maintenance therapy of duodenal ulcer patients with 400 mg cimetidine an increase of the postprandial gastrin output can be observed after 12 months treatment, whereas basal serum gastrin, antral G-cell density and gastric acid secretion remained unchanged. These results suggest that the effects observed during antacid treatment can not be related to an increase in gastric pH and may rather reflect a pH independent direct action of Magaldrate on the antral G-cell.

Adult↗
PubMed1982

Adrenergic and cholinergic interactions in rat gastric somatostatin and gastrin release.

The interactions of adrenergic and cholinergic influences on the gastric D cell were studied using an isolated perfused rat stomach in vitro. The sevenfold increase in the release of somatostatin-like immunoreactivity (SLI) in response to isoproterenol (4 . 10(-8) M) was dose-dependently inhibited by acetylcholine (10(-5) to 10(-8) M) whereas gastrin levels increased in a dose-dependent manner. Both inhibition of stimulated SLI and augmentation of gastrin release were completely abolished by atropine (10(-6) M). Isoproterenol (8 . 10(-9) M)-induced stimulation of SLI secretion was not altered by atropine. Antral exclusion completely eliminated gastrin secretion but basal and beta-adrenergic stimulated SLI release was not influenced. It is concluded that (1) cholinergic agonism reverses the stimulatory action of adrenergic agonists on the D cell, and (2) SLI from the rat stomach in vitro originates almost exclusively in the fundic region.

Acetylcholine↗
PubMed1982

Exocrine pancreatic function in insulin-dependent diabetes mellitus.

Exocrine pancreatic function was studied in patients with long-standing insulin-dependent diabetes mellitus using the secretin-pancreozymin test (n = 53), and estimation of immunoreactive trypsin (n = 43) and pancreatic isoamylase (n = 43). The secretin-pancreozymin test was abnormal in 23 patients (43%). The abnormalities found were a decreased output of lipase (37%), amylase (36%) or trypsin (26%) and bicarbonate (15%). Serum immunoreactive trypsin was below normal in only 6 (14%) and pancreatic isoamylase in 29 (67%) patients. There was no correlation between impairment of the secretin-pancreozymin test and decreased serum enzyme levels. It is concluded that an impairment of exocrine pancreatic function is frequent in insulin-dependent diabetics but that a decrease in serum enzymes, especially in pancreatic isoamylase, does not reflect an impairment of pancreatic function in these patients.

Adult↗
PubMed1982

Effect of food deprivation on rat gastric somatostatin and gastrin release.

The influence of food deprivation on the release of somatostatin and gastrin from the rat stomach was investigated using an isolated, vascularly perfused rat stomach preparation. Basal and acetylcholine-stimulated gastrin release were significantly lower after a 3 day starvation, whereas the inhibitory effect of acetylcholine and the stimulatory effect of glucagon on somatostatin secretion were not influenced by fasting. In dose-response studies, isoproterenol dose-dependently stimulated somatostatin secretion. The increases were similar in both groups fasted for 12 and 72 h. Gastrin release remained at basal levels. Bombesin dose-dependently increased gastrin secretion; this stimulatory effect on the G cell was significantly reduced after a 72-h starvation. Somatostatin secretion was only weakly stimulated by high concentration of bombesin revealing no effect of fasting. Somatostatin content of the nonperfused stomach declined from 57 +/- 4 pmol/stomach in fed controls to 36 +/- 3 pmol/stomach after a 72-h fast. Antral gastrin concentration decreased by 42% in a 3-day fasting period. It is concluded that rat gastric somatostatin release in vitro is--in contrast to gastrin--not altered by food deprivation while the somatostatin content in gastric tissue declined during fasting.

Acetylcholine↗
PubMed1981

[Myoglobinuria in malabsorption after small bowel resection].

A patient with subtotal small bowel resection after mesenterial vein thrombosis presented with muscular weakness and pain. An increase in the activities of enzymes of muscular origin and of myoglobin in serum was found and myoglobinuria was detected. Muscle damage in this patient is attributed to electrolyte disturbances following extensive small bowel resection.

Aged↗
PubMed1981

Gastric inhibitory polypeptide stimulated secretion of somatostatinlike immunoreactivity from the stomach: inhibition by acetylcholine or vagal stimulation.

The possible involvement of gastric somatostatinlike immunoreactivity (SLI) in the acid inhibitory action of gastric inhibitory polypeptide (GIP) was studied in an isolated perfused rat stomach. GIP, in a dose of 5 or 50 ng/mL, caused a 4- and 12-fold increase in SLI secretion, respectively. At the higher dose level the stimulated secretory rate declined throughout the perfusion suggesting that secretion exceeded the capacity to synthesize SLI under excessive GIP stimulation. Acetylcholine (10 microM) or vagal stimulation (7 V, 10 Hz, 5 ms) completely inhibited GIP-stimulated SLI secretion. It is therefore proposed that the acid inhibitory activity of GIP is probably mediated via release of gastric SLI and this action is under cholinergic control.

Acetylcholine↗