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Biomedical subjects

H Goebell

Publications and source records attributed to H Goebell.

At least 235 records · Page 13Linked to original sources
PubMed1983

Natural purified porcine gastric inhibitory polypeptide (GIP) stimulates exocrine pancreas secretion due to contamination with a cholecystokinin-like substance.

The effects of purified natural gastric inhibitory polypeptide-enterogastrone III (GIP-EG III) and a fraction which is further purified by high pressure liquid chromatography (GIP-HPLC) were investigated on the endocrine and exocrine isolated perfused pancreas of rats. At the dose of 5 ng/ml used for both GIP preparations, only GIP-EG III significantly stimulated volume and amylase secretion of the exocrine pancreas. The response of insulin release to stimulation by GIP-EG III or GIP-HPLC was not significantly different. In the presence of cholecystokinin-octapeptide (CCK-8) at a concentration which gave half-maximal stimulation of amylase secretion, GIP-EG III almost doubled the response of the exocrine pancreas, whereas GIP-HPLC had no additional effect. CCK-8 alone significantly increased total insulin output under hyperglycemic conditions. We conclude that porcine GIP purified by gel chromatography contains a CCK-like substance which can be removed by further purification on high pressure liquid chromatography without affecting the insulinotropic activity. Some of the reported effects of GIP could be due to contamination.

Amylases↗
PubMed1983

Beer and wine but not whisky and pure ethanol do stimulate release of gastrin in humans.

In humans, the action of ethanol on gastrin release is still unclear and that of alcoholic beverages greatly unknown. We studied the effect of a drink of various concentrations of pure ethanol and several commonly ingested alcoholic beverages on plasma levels of immunoreactive gastrin in 6 healthy human volunteers and compared the results to a protein-rich meal. A drink of distilled water (250 ml) and of pure ethanol (250 ml or 125 ml in the case of 40% v/v ethanol) in concentrations (4, 10, 20 and 40% v/v) normally present in beer, wine, liquor and whisky did not stimulate plasma gastrin levels above basal. Of the alcoholic beverages given only whisky (125 ml) did not stimulate gastrin release. Beer, red and white wine (250 ml each) caused a rapid increase in plasma gastrin concentrations with a peak at 15-20 min, basal levels being reached 60 min after starting the drink. The 60-min integrated plasma gastrin response to beer, red and white wine was about 50% of the gastrin response to the protein-rich (steak) meal (883 +/- 297 pmol X min X 1(-1); mean +/- SE). A drink of 250 ml of white wine together with the meal did not cause a significantly higher integrated gastrin response than the protein meal with 250 ml of distilled water. We conclude that commonly ingested alcoholic beverages such as beer, red and white wine, but not whisky, are potent stimulants of gastrin release in humans. The ethanol content of these beverages cannot be responsible for the increase in plasma gastrin levels, since oral ingestion of pure ethanol in equivalent concentrations and amounts did not elicit a rise in plasma gastrin levels. Some unknown ingredients present in beer and wine are most likely responsible for the gastrin release by both alcoholic beverages.

Adult↗
PubMed1983

Calcium secretion from the feline pancreas. Influence of hormonal and cholinergic secretagogues and of serum calcium.

The influences of secretagogues and of elevated serum calcium concentrations on the calcium secretion from the cat pancreas have been studied in vivo. During a high and constant fluid secretion rate evoked by a background infusion of secretin, additional infusions of both cholecystokinin-pancreozymin and urecholine led to a dose-dependent increase in calcium secretion in pancreatic juice parallel to the rise of protein. The amount of calcium in pancreatic juice associated to 1 mg protein (18.3 nmol/mg protein) calculated from regression analysis was independent of dose or kind of stimulus used. The protein-independent pancreatic juice calcium fraction was 0.184 mM in normocalcemia. During an episode of hypercalcemia produced by an intravenous calcium infusion, the protein-independent calcium fraction was increased and correlated linearly to the serum calcium concentration. We conclude that pancreatic juice calcium consists of two major fractions, one being associated with the enzyme protein and stimulated by secretagogues, and the other being protein independent and directly dependent on the extracellular calcium concentration.

Animals↗
PubMed1983

Excretion of azlocillin and mezlocillin by the normal pancreas and in acute pancreatitis in dogs and rats.

Dogs and rats were studied to evaluate the excretion of two new acyl-ureidopenicillins, azlocillin and mezlocillin, in the pancreatic fluid. After intravenous administration of 55 mg X kg-1 of either drug, an extremely low concentration (less than 3.0 micrograms X ml-1) of both antibiotics was measured in pancreatic juice of conscious dogs. In rats, both azlocillin and mezlocillin were excreted by the pancreas in bactericidal concentrations (greater than 10 micrograms X ml-1) during the first 15 min following their injection. In anesthetized dogs and rats in which acute pancreatitis was induced by injection of sodium taurocholate into the main pancreatic duct, the tissue concentration of mezlocillin (55 mg X kg-1 i.v.) was significantly higher than in the pancreatic tissue of control animals. In both instances, bactericidal concentrations of mezlocillin were measured in the pancreatic tissue. During the first 30 min following its injection, the concentration of mezlocillin was about five times higher in inflammed pancreatic tissue than in the normal pancreas (dogs: 44 +/- 14 vs. 5 +/- 3 micrograms X g-1 tissue; rats: 67 +/- 10 vs. 13 +/- 2 micrograms X g-1). These data indicate that (1) azlocillin and mezlocillin are excreted in bactericidal concentrations by the normal pancreas only in rats but not in dogs, and (2) in both species, bactericidal concentrations of mezlocillin can be observed in the normal pancreatic tissue and in acute pancreatitis; its concentration being significantly higher in acute pancreatitis than in controls.

Acute Disease↗
PubMed1983

Glucose-dependent insulinotropic action of cholecystokinin octapeptide in the isolated perfused rat pancreas.

Whether cholecystokininoctapeptide (CCK-8) stimulates insulin secretion at submaximal or supramaximal levels for pancreatic exocrine secretion was investigated. CCK-8 was delivered to the isolated perfused rat pancreas by a linear gradient ranging from 0 to 1,100 or 0 to 220 pg/ml at two different glucose concentrations. At 2.8 mM glucose CCK-8 was not insulinotropic even at supramaximal stimulation for exocrine pancreatic secretion. At 15.8 mM glucose CCK-8 was insulinotropic starting already at concentrations which were submaximal for stimulation of exocrine pancreatic secretion. It was concluded that CCK-8 warrants consideration as a hormone involved in the enteroinsular axis.

Animals↗
PubMed1983

Effect of atropine on pancreatic bicarbonate output and plasma concentrations of immunoreactive secretin in response to intraduodenal stimulants.

In conscious dogs with gastric and pancreatic Thomas fistulas we studied the effect of atropine (50 micrograms kg-1 intravenously) on pancreatic bicarbonate output and plasma concentrations of immunoreactive secretin in response to intraduodenal bolus injections of HCl (0.75 mmol), L-tryptophan (1 mmol), and sodium oleate (1 mmol). The 10-min integrated bicarbonate response to HCl was 1.7 times greater than the response to oleate and 2.8 times greater than that to tryptophan. Atropine significantly (p less than 0.05) depressed the 10-min integrated bicarbonate response to HCl, oleate, and tryptophan by 67%, 79%, and 61%, respectively. HCl and oleate, but not tryptophan, significantly increased plasma secretin concentrations over basal levels. Atropine did not significantly alter basal plasma concentrations of secretin or the 10-min integrated plasma secretin response to HCl and oleate. We conclude that 1) intraduodenal tryptophan stimulates pancreatic bicarbonate secretion by an atropine-sensitive mechanism, release of secretin not being involved, and 2) in the presence of atropine the depressed pancreatic bicarbonate response to HCl and oleate is not due to decreased release of endogenous secretin.

Animals↗
PubMed1983

[Systolic time intervals in chronic calcifying pancreatitis caused by alcohol abuse].

Systolic time intervals corrected for heart rate were measured non invasively in 12 male patients (32 to 59 years) with chronic calcifying pancreatitis of alcoholic origin and compared with 24 normal subjects without evidence for chronic alcoholism or heart disease. Systolic time intervals (in detail: the time from the beginning of QRS to the first heart sound (QS1), the isovolumic contraction time (IVCT), the total electromechanical systolic interval (QS2c), the pre-ejection period (PEPc), the left ventricular ejection time (LVETc) and the ratio PEPc/LVETc) in patients with chronic calcifying pancreatitis were not different when compared with healthy man. Therefore we conclude, that the amount of alcohol that induced a chronic calcifying pancreatitis was not able to alter systolic time intervals as seen in an alcoholic cardiomyopathy.

Adult↗
PubMed1982

Lack of effect of luteinizing hormone-releasing hormone on pancreatic exocrine secretion and release of gastrin and pancreatic polypeptide in dog.

In 7 conscious dogs with gastric and duodenal Thomas fistulas we studied the effect of an intravenous bolus injection of luteinizing hormone-releasing hormone (LHRH, 100 microgram) on pancreatic bicarbonate and protein secretion stimulated by an intravenous infusion of secretin (500 ng kg-1 hr-1) and on plasma concentrations of pancreatic polypeptide (PP) and gastrin. LHRH did not significantly alter pancreatic bicarbonate and protein output in response to secretion and plasma levels of gastrin and PP as measured by radioimmunoassay. The lack of any significant influences of intravenous LHRH on exocrine pancreatic secretion does not exclude an effect of LHRH on pancreatic bicarbonate and enzyme secretion via paracrine delivery.

Animals↗
PubMed1981

Effects of clanobutin on pancreatic secretion in vitro.

The effects of clanobutin (4-[4-chloro-N-(4-methoxyphenyl)-benzamido]butyric acid) were investigated on two in vitro pancreatic preparations. In rat pancreatic lobules clanobutin (7.2 mM) stimulated the secretion of amylase and radiolabeled proteins to the same or higher extent as did CCK-PZ and carbachol in maximally active doses, but with a delay of 1-2 h. In the isolated rabbit pancreas clanobutin (3.3 mM) stimulated protein secretion about half as much as did carbachol, but without significant delay. The effect of clanobutin on protein secretion was prevented by prior application of carbachol, was not affected by the omission of Ca2+ from the medium and was only partly inhibited by the presence of atropine (0.1 mM). Prior addition of clanobutin did not prevent the effects of carbachol on enzyme secretion. In addition, clanobutin (3.3 mM) inhibited fluid secretion in the rabbit pancreas by about 50 percent; the inhibition was reversible. No effects on paracellular permeability were found with sucrose used as test substance. The findings indicate that clanobutin has opposite effects on enzyme and fluid secretion by rat and rabbit pancreas, which are not due to circulatory effects.

Amylases↗
PubMed1981

[Endocrinologic findings in Crohn's disease].

In 45 patients with radiologically and endoscopically/histologically proven Crohn's disease the partial functions of the anterior pituitary gland were measured prior to steroid therapy. No deficiencies were observed with respect to cortico-, thyro-, gonado-, and somatotropic functions. In 25 out of 40 patients (63%) the typical diurnal rhythm of cortisol secretion was absent when assessed by a distinctly elevated 6 p.m. cortisol serum level. In about one fourth of 22 patients T3-RIA was reduced, indicating deficiency of conversion from T4 to T3. Six (43%) out of 14 males showed reduced basal testosterone levels at 8 a.m. and 6 p.m. which, in 4 out of 14 cases, did not increase sufficiently in response to HCG. The basal LH-level was elevated in 9 (50%) of 18 males. The lack of diurnal rhythm of cortisol secretion and primary insufficiency of Leydig's cells did not correlate with the activity of the disease.

Adolescent↗
PubMed1981

Effects of truncal vagotomy and antrectomy on bombesin-stimulated pancreatic secretion, release of gastrin, and pancreatic polypeptide in the anesthetized dog.

The short-term effects of truncal vagotomy and antrectomy on bombesin-stimulated pancreatic secretion and release of gastrin and pancreatic polypeptide (PP) were studied in 18 anesthetized dogs. Together with an intravenous infusion of secretin (250 ng/kg/hr) bombesin (500 ng/kg/hr) was given before and after truncal vagotomy, antrectomy, and sham operation (N = 6 dogs per group). Peak incremental pancreatic protein output in response to bombesin was about 2-3 times higher before than after the different surgical procedures (tachyphylaxis). Neither truncal vagotomy nor antrectomy significantly altered the pancreatic protein response to bombesin when compared with sham operation. Bombesin produced a mean 1-hr increase over basal of 196 pM for gastrin, which was abolished by antrectomy but not appreciably affected by truncal vagotomy and sham operation. The mean 1-hr increment (207 pM) for PP in response to bombesin was not changed by truncal vagotomy, antrectomy, and sham operation. This study shows in the anesthetized dog that exogenous bombesin stimulates release of PP as well as gastrin; that the release of gastrin by bombesin is not vagally dependent; that neither truncal vagotomy nor antrectomy alter the release of PP by bombesin; and that the action of bombesin on pancreatic protein secretion does not depend on release of gastrin or on intact vagal nerves.

Animals↗
PubMed1981

Effect of atropine on pancreatic response to HCl and secretin.

In dogs with gastric and pancreatic fistulas, we studied the effect of atropine on the pancreatic secretory response to secretin and intestinal HCl. Atropine sulfate (20 micrograms.kg-1.h-1 iv) significantly depressed basal bicarbonate and protein output. Atropine depressed bicarbonate responses to low doses (62.5, 125, 250, and 500 ng.kg-1.h-1) of secretin but had no significant effect on responses to high doses (1,000 and 2,000 ng.kg-1.h-1). Secretin, with or without atropine, did not stimulate pancreatic protein output above basal. Atropine depressed bicarbonate responses to low loads (3, 6, and 12 mmol.h-1) of HCl but had no significant effect on responses to high loads (12, 24, and 48 mmol.h-1). Intraduodenal HCl produced a dose-dependent increase in protein output. Atropine abolished protein responses to low loads (3 and 6 mmol.h-1) but did not affect responses to high loads (24 and 48 mmol.h-1) of HCl. These findings are compatible with the hypotheses that a) endogenous cholinergic activity augments the pancreatic bicarbonate response to secretin, and b) the pancreatic protein response to intraduodenal HCl is, at least in part, mediated cholinergically.

Animals↗