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Biomedical subjects

H Goebell

Publications and source records attributed to H Goebell.

At least 91 records · Page 5Linked to original sources
PubMed1987

GIP potentiates CCK stimulated pancreatic enzyme secretion: correlation of anatomical structures with the effects of GIP and CCK on amylase secretion.

Utilizing scanning electron microscopy and isolated, vascularly perfused rat pancreas, we studied the angioarchitecture and the effect of the insulinotropic hormone, gastric inhibitory polypeptide (GIP), on cholecystokinin (CCK)-stimulated exocrine secretion. We tried to correlate the microcirculation with the physiological effect of insulin on the pancreatic secretion in the same species. We found a vascular pattern consisting of direct insuloacinar connections, a venous drainage system of islets, and a direct arterial supply of acini. GIP at a concentration as low as 2 ng/ml or exogenous rat insulin potentiated CCK-stimulated pancreatic enzyme secretion. To have similar effects as insulin which is endogenously released by GIP, about 30 times more exogenous rat insulin has to be infused. We conclude that based on the angioarchitecture, insulinotropic hormones like GIP could link the metabolic and the digestive function of the pancreas.

Amylases↗
PubMed1987

In vitro stimulation of pancreatic enzyme discharge by calcium.

The mechanism for acute hypercalcaemia increasing pancreatic enzyme secretion is unknown. To determine if raised extracellular calcium concentrations can directly stimulate pancreatic enzyme output, we measured discharges of pulse labelled protein and chymotrypsin from isolated cat pancreatic lobules in the presence of normal and raised calcium concentrations. Incubation in 5.0 mmol/l calcium increased discharges of pulse labelled protein (four fold), chymotrypsin (2.5 fold) and amylase (2.2 fold), compared with control experiments with 2.5 mmol/l calcium (p less than 0.001). This effect was similar to the maximal effect of carbachol or caerulein. Compared with 5.0 mmol/l calcium, incubation at the higher calcium concentration of 10.0 mmol/l induced similar discharges of chymotrypsin and amylase, whereas the increase in discharge of pulse labelled protein was smaller (p less than 0.01). The effects of raised calcium were not altered by atropine. Incubation in a high calcium medium did not impair pancreatic acinar response to subsequent stimulation with carbachol, but incubation in hypothermia abolished the effects of high calcium concentrations, suggesting that increased enzyme discharge is caused by stimulation of secretion not to cell damage. These data are consistent with a direct stimulatory effect of raised extracellular calcium concentrations on pancreatic acinar cell function.

Animals↗
PubMed1987

Detection of cholecystokinin-58 in human blood by inhibition of degradation.

Although cholecystokinin-58 (CCK-58) is a major molecular form stored in the intestine, it has not yet been shown to be released into the circulation. This report describes in vitro degradation of CCK-58 in human blood and plasma and the molecular forms detected when this degradation is inhibited. After incubation of CCK-58 for 150 min between 20 and 24 degrees C, approximately 60% of immunoreactivity recovered was degraded to smaller immunoreactive forms. Storage of the 150-min incubate at -20 degrees C for 3 days greatly increased the observed degradation to 85%. When CCK-58 was added in vitro to blood, similar degradation occurred. Degradation of CCK-58 could be inhibited by addition of acid. Blood was obtained 1 h after a test meal designed to stimulate CCK release. The pH was lowered during collection and processing of blood and plasma to inhibit in vitro degradation of cholecystokinin. This method permitted the detection of significant amounts of CCK-58 in circulation.

Cholecystokinin↗
PubMed1987

Effect of rioprostil, a synthetic prostaglandin E1 on meal-stimulated gastric acid secretion and plasma gastrin levels in humans.

The effects of rioprostil (a newly developed synthetic prostaglandin E1 analogue) on meal-stimulated gastric acid secretion was evaluated in 8 healthy human volunteers. Gastric acid output was measured by intragastric titration on 4 different occasions. The following procedure was invariably employed: after a basal period of 45 min, 5 peptone meals (8%, 500 ml each) were given intragastrically in 45-min intervals and gastric acid output was measured continuously. 45 min after the first meal, either placebo or 150, 300 or 600 micrograms of rioprostil were given intragastrically in a randomized order and on different days. 15 min later, the second meal was given and intragastric titration continued. Rioprostil caused a dose-dependent inhibition of the 3-hour integrated gastric acid response to the peptone meals. The percentage of inhibition was 41, 68 and 79%, respectively, for 150, 300 and 600 micrograms of rioprostil. Whereas the inhibition by the two highest doses was statistically significant, this was not the case for the lowest dose of rioprostil. The integrated 3-hour plasma gastrin response to the peptone meals was not significantly changed by any of the doses of rioprostil. No significant adverse effects were observed with rioprostil.

Adolescent↗
PubMed1987

[Interdigestive motility and secretion of the gastrointestinal tract].

In the fasting state, the digestive tract is not inactive but displays periodic motor and secretory activity. Each gastrointestinal motility cycle can be divided into specific phases of activity: a period of inactivity (phase I), followed by a longer period of irregular activity (phase II) and by a brief, conclusive period (phase III) of maximal, rhythmic contractions, the migrating motor complex (MMC), which migrates from the gastroduodenal region to the distal small bowel within one motility cycle. A short, inconstant transition segment between phases III and I is termed phase IV. Lower esophageal, gallbladder and sphincter of Oddi motilities are also linked to this functional cycle. In contrast, colonic motility follows independent patterns. Closely correlated to upper gastrointestinal motility are secretory activities: Output rates of gastric, pancreatic and bile secretions increase and decrease periodically, in concert with upper gastrointestinal motor activities. The physiologic role of periodic interdigestive activity is not fully understood. It is probably important for regular mechanical and enzymatic cleansing ot the gastrointestinal lumen and may serve to remove indigestible and/or foreign material, to prevent bacterial overgrowth or pathologic activation of pancreatic enzymes, and to revert duodeno-gastric and ceco-ileal refluxes. Control of the interdigestive cycle and mechanisms of motor/secretory coupling have been only partly uncovered; however, recent findings suggest that interactions between vagal and intrinsic cholinergic pathways and gastrointestinal hormones may play pivotal regulatory roles.

Digestion↗
PubMed1986

Gastroparesis after radiation. Successful treatment with carbachol.

Following abdominal radiation, a 16-year-old male developed persistent vomiting, metabolic alkalosis, and cachexia secondary to gastric stasis, atony, and dilatation in the absence of mechanical obstruction. Fluoroscopically and manometrically, antral motility was found to be severely impaired. Antral motor activity was not influenced by metoclopramide, but stimulated by carbachol. During oral maintenance carbachol therapy, gastric emptying of food was restored and sufficient oral nutrition could be resumed. The improvement persisted even after termination of therapy four months later. Systematic investigations on the effects of abdominal radiation on gastrointestinal motility appear to be necessary.

Adolescent↗
PubMed1986

Bile secretion in acute and chronic hypercalcemia in the cat.

The reported coincidence of primary hyperparathyroidism and cholelithiasis led us to investigate the effects of acute and chronic hypercalcemia on bile secretion in cats. Acute hypercalcemia (6-7 mmol/liter) was induced by an intravenous calcium infusion. Chronic hypercalcemia (3-4 mmol/liter) was induced and maintained for 8-10 weeks by treatment with subcutaneous vitamin D3, oral dihydrotachysterol, and feeding a calcium-rich diet. Bile secretion was then studied in acute experiments. We found that calcium concentrations in serum and hepatic bile were similar during all experimental normo- or hypercalcemic conditions (y = 1.12x - 0.85; r = 0.76). Biliary volume outputs were significantly decreased during both acute (P less than 0.002) and chronic (P less than 0.05) hypercalcemia compared with normocalcemic controls. Acute hypercalcemia also decreased total bile acid outputs (P less than 0.05), but had no effect on biliary bile acid concentrations. The inhibitory effect of acute hypercalcemia on biliary fluid and bile acid secretion was dose dependent and not antagonized by atropine. These findings suggest that calcium is secreted in hepatic bile at similar concentrations as present in the serum and that elevations of serum calcium concentration inhibit biliary volume and bile acid secretion in cats. Similar effects of hypercalcemia on bile composition in humans might promote calcium salt precipitation in bile.

Acute Disease↗
PubMed1986

Fecal bile acid excretion pattern in cholecystectomized patients.

The fecal bile acid excretion pattern was investigated in 25 cholecystectomized and 26 noncholecystectomized patients as a measure for the exposure of the colonic mucosa to bile acids. Separation of free, conjugated, and sulfated bile acids was achieved by liquid-gel chromatography using DEAP Sephadex LH-20 and quantification of individual bile acids by gas-liquid chromatography. Total bile acid concentration was higher in cholecystectomized (5.33 +/- 0.71 mg/g) than in noncholecystectomized patients (3.69 +/- 0.65 mg/g). Deoxycholic acid excretion was elevated in cholecystectomized patients in three aspects: the concentration of deoxycholic acid was higher (2.92 +/- 0.39 mg/g and 1.71 +/- 0.35 mg/g, respectively), its percentage proportion of total bile acids was increased (53.9 +/- 2.8% and 41.4 +/- 3.1%, respectively), and its daily output was twice as large as that in patients without previous cholecystectomy (63.2 +/- 11.5 and 32.9 +/- 5.9 mg/day, respectively).

Adult↗