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Biomedical subjects

H Goebell

Publications and source records attributed to H Goebell.

At least 73 records · Page 4Linked to original sources
PubMed1988

Effects of camostat, a synthetic protease inhibitor, on endocrine and exocrine pancreas of the rat.

The effects of chronic oral treatment of rats with 400 mg/kg body weight camostat, a synthetic protease inhibitor, on weight gain and both pancreatic exocrine and endocrine secretion were studied and compared with pair-fed controls. Administration of camostat was found to result in a lower weight gain than in untreated rats fed ad libitum because of reduced food intake. The pancreas of treated rats showed hypertrophy and hyperplasia with significantly higher total contents of amylase, lipase, trypsinogen and chymotrypsinogen than that of pair-fed controls. The specific activity of lipase, trypsinogen and chymotrypsinogen remained unchanged but the specific activity of amylase was significantly lower than in pair-fed controls. Stimulation of pancreatic enzymes with CCK 8 in treated rats resulted in a greater output of proteases, no difference in secretion of lipase and a lower secretion of amylase than in pair-fed rats. Glucose-dependent insulin secretion was also significantly lower in camostat-treated rats than in controls. This effect could be reversed by gastric inhibitory polypeptide. After termination of treatment with camostat all enzymes were normalized within 14 d. Our results on the hypertrophied pancreas of rats suggest preferential synthesis and secretion of protease at the expense of amylase and diminished sensitivity of insulin to stimulation by glucose. All effects of camostat on the pancreas were reversible.

Amylases↗
PubMed1988

Pancreatic and gastric responses to gastric versus jejunal beer in humans.

To investigate the influence of beer on gastric and pancreatic secretion, 14 fasted volunteers were studied on two different days. A multilumen intestinal tube allowed measurement of intraluminal pressures and collection of gastric and duodenal juices. Seven subjects received in random order 250 ml of either beer or glucose (5.6%, w/v) intragastrically; seven other subjects received these intrajejunally. After 15 min, 48 +/- 8% of beer and 47 +/- 6% of glucose were emptied into the duodenum. Intragastric beer induced a nearly sevenfold increase in gastric acid output as compared with glucose (16.3 +/- 2.9 mmol/h versus 2.5 +/- 0.6 mmol/h; p less than 0.05), intrajejunal beer induced a nearly threefold increase (5.1 +/- 0.8 mmol/h versus 1.7 +/- 0.3 mmol/h). The stimulated gastric acid output was threefold higher after intragastric than after intrajejunal beer. Trypsin output was slightly but significantly (p less than 0.05) stimulated by intragastric beer as compared with glucose (4,639 +/- 460 U/h versus 3,628 +/- 399 U/h) and nearly threefold by intrajejunal beer (2,579 +/- 455 U/h versus 849 +/- 181 U/h) (p less than 0.05). Trypsin response to intragastric beer was 1.8 times higher than after intrajejunal beer (p less than 0.05). Intragastric beer induced a nearly ninefold increase of the 1 h integrated plasma gastrin response as compared with glucose (998 +/- 347 pM min vs 115 +/- 70 pM min) (p less than 0.05). Intrajejunal beer and glucose did not release gastrin. We conclude that both intragastric and intrajejunal beer stimulate gastric acid and pancreatic enzyme secretion; intragastric beer being a more potent stimulant. Gastrin might partially mediate the responses to intragastric but not to intrajejunal beer.

Adult↗
PubMed1988

Effects of somatostatin-14 on gastric and pancreatic responses to hormonal and neural stimulation using an isolated perfused rat stomach and pancreas preparation.

To study the role of somatostatin in the regulation of pancreatic and gastric functions, a combined isolated rat stomach and pancreas preparation was developed. This model allowed simultaneous measurements of exocrine and endocrine secretion from the pancreas and gastrin secretion from the stomach. Somatostatin was applied either by a linear gradient or by constant infusion with one concentration in the presence of cerulein, secretin, electric vagal activity, or acetylcholine. Somatostatin did not influence exocrine pancreatic secretion irrespective of what substance was stimulated. In contrast, somatostatin significantly inhibited glucose-dependent insulin and gastrin secretion, either basal or stimulated by vagal activity or acetylcholine. Acetylcholine-induced gastrin secretion was more sensitive to inhibition by somatostatin than insulin. We conclude that in an isolated perfused organ system somatostatin has potent inhibitory effects on endocrine pancreas and stomach but has no effect on exocrine pancreatic volume and enzyme secretion.

Amylases↗
PubMed1988

Differential sensitivity of rat exocrine and endocrine pancreas to cyclosporine.

The effect of 5, 10, and 20 mg/kg bw cyclosporine on rat endocrine and exocrine pancreatic function was studied. Glucose-dependent insulin secretion from the endocrine pancreas was shown to be significantly impaired 8 days after cyclosporine was given once daily at a dose as low as 5 mg/kg. CCK-8-stimulated amylase and lipase secretion were less sensitive to the noxious effect of cyclosporine being impaired at a dose of 10 mg/kg. Trypsin secretion was shown to be impaired at 20 mg/kg cyclosporine only. Our results demonstrate that cyclosporine causes dose-dependent impairment of both pancreatic endocrine and exocrine functions: the endocrine pancreas being more sensitive to the noxious action than the exocrine pancreas.

Amylases↗
PubMed1988

Prevention of toxic effects of cyclosporin on pancreatic B-cells of rats by Rioprostil, a new prostaglandin analogue.

Cyclosporin 5, 10, and 20 mg/kg bw was given to rats once daily intragastrically and caused a dose dependent, significant decrease of glucose dependent insulin release from the arterially perfused isolated pancreas, without affecting animal behaviour, weight gain, microscopic appearances of the pancreas, or kidney function. Subcutaneous injection of a new synthetic prostaglandin analogue Rioprostil 7.5 micrograms/kg bw twice daily completely prevented the effect of cyclosporin 5 mg/kg bw and protected significantly against the effects of cyclosporin 10 and 20 mg/kg bw.

Animals↗
PubMed1988

Large bowel cancer risk in cholelithiasis and after cholecystectomy. Postmortem study.

To assess the large bowel cancer risk in cholelithiasis (CL) and after cholecystectomy (CE), the results of 11,828 autopsies were analyzed. 1,705 cases with CL and 380 with CE could be identified. Randomly selected cases matched for sex and age were used as controls. In CL and CE 61 cancers were observed compared with 53 in controls, the relative risk (RR) being 1.2. The risk ratio for the subgroups (CL, CE) was also 1.2. In contrast to women, there was a positive association (RR 1.7) between cancer and CL in men, in whom no risk increase was found after CE. In cases with CL and CE an elevated risk of developing proximal large bowel cancer was observed for both sexes (RR 1.7 in males and 1.4 in females). As regards distal cancer, no such relationship was observed in women (RR 0.83) whereas an increased risk was found in men (RR 2.3). The results of this study are in favor of a positive association between CL and CE and the risk of developing large bowel cancer.

Aged↗
PubMed1988

[Treatment of chronic non-secretory diarrhea in ileostomy with the long-acting somatostatin analog SMS 201-995].

A patient with chronic refractory non-secretory diarrhea following ileostomy was treated with the long acting somatostatin analogue SMS 201-995. Under treatment with somatostatin stool weights were drastically reduced and electrolyte dysbalance was normalized within a few days. This case report shows that somatostatin is also therapeutically effective in non-secretory diarrhea.

Colectomy↗
PubMed1988

[Acute manifestations in Crohn disease and ulcerative colitis. Conservative treatment of acute situations].

Ulcerative colitis (UC) and Crohn's disease (CD) can lead to perforation, abscesses and peritonitis. In such cases conservative treatment should only be secondary to surgery, whereas intensive conservative treatment is needed from the very start in toxic megacolon. The decision to operate must be made within 24-48 h. Partial or complete intestinal obstruction is frequently encountered in CD patients if the ileum is involved. Prednisone treatment can sometimes reverse this condition when combined with parenteral nutrition. Treatment of acute exacerbations of UC and CD is essentially conservative and consists of salazosulfapyridine or 5-aminosalicylic acid and prednisone.

Acute Disease↗
PubMed1987

Cholecystokinin-58 is the major circulating form of cholecystokinin in canine blood.

Cholecystokinin-58 (CCK-58) is the largest and most abundant, biologically active form of cholecystokinin in canine intestinal mucosa. Despite the high amounts in mucosa, CCK-58 has not been detected in significant amounts in the circulation. The release of CCK-58 into the peripheral blood in response to an intraduodenal perfusion of sodium oleate (9.0 mmol h-1) was studied in seven conscious dogs. Plasma (50 ml) was obtained before and after endogenous stimulation by a newly developed method that prevents in vitro degradation of large cholecystokinins. The relative abundance of immunoreactive forms of CCK was studied by high pressure liquid chromatography (HPLC) which separated the gastrin and CCK forms. Column eluates were measured with an antibody which recognizes the intact carboxyl terminus of both gastrin and CCK. Cholecystokinin immunoreactivity increased over basal in plasma by 7 fmol/ml after intraduodenal perfusion with sodium oleate. The most abundant form of stimulated cholecystokinin immunoreactivity eluted on HPLC in the position of CCK-58 (63% of total immunoreactivity found). Since CCK-58 is biologically active and is the most abundant circulating form, it should play an important role in the physiology of cholecystokinin.

Animals↗
PubMed1987

Possible mode of action of 5-aminosalicylic acid.

Despite the extensive use of sulfasalazine (SAS) and/or 5-aminosalicylic acid (5-ASA) in patients with inflammatory bowel disease and, more recently, rheumatoid arthritis, their mode of action has not been elucidated so far. None of the numerous pharmacological and biochemical effects described, including immunosuppressive, antifolate, and modulatory actions on lymphocyte and leukocyte functions, could be defined unequivocally as mediating their beneficial activity. Recently, interest has focused on actions of SAS and 5-ASA on the various enzymes of the arachidonic acid cascade. Mucosa of patients with inflammatory bowel disease generates excessive amounts of cyclooxygenase products such as prostaglandins (PG) as well as 5-lipoxygenase products such as leukotriene (LT) B4 and sulfidopeptide-LT. Both PG and LT exert proinflammatory actions and are potentially important mediators of mucosal inflammation. SAS and 5-ASA, however, have been found to inhibit PG synthesis under certain experimental conditions only, while increasing PG formation under other conditions. While SAS was found to inhibit colonic LTB4 synthesis, 5-ASA was reported to selectively affect the cyclooxygenase pathway of arachidonate metabolism in this tissue. Our results demonstrate that, like the parent compound, the metabolite 5-ASA in a dose-dependent manner inhibits release of LTB4 and sulfidopeptide-LT from normal human colonic mucosa (IC50 3.5 and 3.7 mmol/liter, respectively). Indomethacin, which has no efficacy in the treatment of patients with inflammatory bowel disease, on the other hand, selectively inhibited PGE2 formation in normal and inflamed colonic mucosa (IC50 1.7 and 1.0 mmol/liter, respectively) without reducing synthesis of LTB4 or sulfidopeptide-LT.(ABSTRACT TRUNCATED AT 250 WORDS)

Aminosalicylic Acids↗
PubMed1987

Action of ethanol and some alcoholic beverages on gastric acid secretion and release of gastrin in humans.

The action of intragastric ethanol in various concentrations (1.4%-40% vol/vol) and of beer, white wine, cognac, and whisky on gastric acid secretion and release of gastrin was studied in healthy humans. Ethanol concentrations of 1.4% and 4% (vol/vol), but not higher, significantly (p less than 0.05) increased gastric acid secretion to 23% and 22%, respectively, of incremental maximal acid output [i.e., observed response to pentagastrin (6 micrograms/kg s.c.) minus basal acid output]. The 1-h incremental gastric acid responses to beer and wine were 96% and 61%, respectively, of incremental maximal acid output. Neither cognac nor whisky had any stimulatory effect. The 1-h incremental gastric acid response to an 8% peptone meal was 40% of incremental maximal acid output, and to peptone plus white wine 77%. Plasma gastrin levels were not altered by ethanol, cognac, and whisky. The 1-h integrated plasma gastrin responses to beer and white wine were 119% and 77%, respectively, of the response to the peptone meal. We conclude that (a) the action of pure ethanol on gastric acid secretion is related to its concentration: concentrations of 1.4% and 4% are moderate stimulants; concentrations of 5%-40% have no effect, or rather an inhibitory effect; (b) beer and white wine, but not whisky and cognac, are potent stimulants of gastric acid secretion; (c) the stimulatory mechanism of low ethanol concentrations is unknown; and (d) nonalcoholic constituents of beer and wine are most likely responsible for the stimulatory actions of both beverages on gastric acid secretion and release of gastrin.

Adult↗