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Biomedical subjects

H Goebell

Publications and source records attributed to H Goebell.

At least 163 records · Page 9Linked to original sources
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↗
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↗