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Biomedical subjects

H Goebell

Publications and source records attributed to H Goebell.

At least 55 records · Page 3Linked to original sources
PubMed1989

Prostaglandin analogue protects pancreatic B-cells against cyclosporin A toxicity.

Cyclosporin A toxicity on pancreatic B-cells and its prevention by rioprostil, a prostaglandin E1 analogue, were studied in the model of the isolated perfused pancreas of rats treated with both compounds for 8 days. At toxic doses of cyclosporin (10 and 20 mg/kg b.wt), the B-cells showed severe hydropic degeneration of the endoplasmatic reticulum and slight degranulation of the B-cells. Accordingly, the insulin secretion was markedly impaired. Administration of rioprostil ameliorated the insulin secretion significantly, but not the ultrastructural changes. At therapeutic levels of cyclosporin (5 mg/kg b.wt), the hydropic degeneration and the drop in insulin secretion were completely prevented by rioprostil. This observation might have therapeutic implications in the treatment of patients, in particular those undergoing pancreatic transplantation.

Animals↗
PubMed1989

[Acute pancreatitis. 2: Treatment of the complicated course].

Owing to its tendency to produce severe local and systemic complications, the hemorrhagic necrotic form of acute pancreatitis is still associated with a high mortality rate. Major local complications are pseudocystic space-consuming masses, arterial bleeding and abscess formation. The major systemic complications include circulatory shock, metabolic disorders, renal failure, respiratory insufficiency and sepsis. Of decisive importance for the prognosis is prophylaxis, early detection, and suitable treatment of these threatening complications, which is achieved on the basis of a combination of standardized basic treatment with problem- and symptom-oriented supplementary treatment. In the present paper, the current prophylactic, diagnostic and therapeutic concepts are described. In addition, a number of invasive measures and the indications for surgery are discussed.

Acute Disease↗
PubMed1989

[Acute pancreatitis. 1: Principles of conservative therapy].

Any patient with suspected acute pancreatitis should be hospitalized in an intensive care unit. Since the course even of an apparently initially uncomplicated attack of pancreatitis can rapidly become severe and life-threatening, close clinical monitoring in accordance with the rules of critical care medicine is necessary. The major therapeutic measures comprise fasting, parenteral replacement of fluid, electrolytes and calories, and pain treatment. The care of patients with acute pancreatitis should be a joint effort on the part of the internist and the surgeon right from the start. At the present time, there is no specific treatment regimen for pancreatitis. Therapeutic concepts of hormonal inhibition of pancreatic secretion, or the inactivation of autodigestive enzymes, have not proved successful, or have not yet been adequately demonstrated to be effective. On resolution of the pancreatitis, an attempt must always be made to identify the cause of cause of the condition, since this forms the basis for further prophylactic and therapeutic consequences.

Acute Disease↗
PubMed1989

[Amyloidosis in Crohn disease. Case reports and review of the literature].

A review of the literature on Crohn's disease with secondary amyloidosis and four own case reports are presented. At least 1% of patients with Crohn's disease develop amyloidosis. The extent of the inflammatory bowel disease seems to have an influence on the occurrence of amyloidosis. The survival time of 40 out of 72 patients was 2.1 years after the onset of diagnosis. The complications induced by the amyloidosis determine the fate of the patients. Therefore the periodical protein determination in urine and the Congo-red-colouring of rectal mucosa after rectoscopy are justified. After the diagnosis of amyloidosis in patients with Crohn's disease the inflammation should be treated consequently, according to the principles of the treatment of the underlying disease. But the resection of the inflammatory bowel should be avoided if the renal function is still sufficient, because frequently there occurs a postoperative renal failure. In the case of renal amyloidosis with a creatinin-clearance of more than 10 ml/min, a therapeutic attempt should be made with 1.0 to 1.5 mg/day of colchicin or 10 g/day dimethylsulphoxid (DMSO) for at least six months. During existing renal failure the proceeding of amyloidosis in other organs is to be expected. The secondary amyloidosis disposes the fate of the patients.

Adult↗
PubMed1989

Clinical relapse of Crohn's disease under standardized conservative treatment and after excisional surgery.

The course of 205 patients with Crohn's disease at one gastroenterological center was studied in patients with conservative drug treatment or with operative management of their disease. The decision for one or the other treatment regimen was made by an interdisciplinary team of gastroenterologists and surgeons. Using life-table analysis the 205 patients showed a clinical relapse rate of 27% after two years and 38% after four years. Clinical relapse was defined by a Crohn's disease activity index (CDAI) over 150. We used a standardized drug regimen of salazosulfapyridin and prednisone; the indication for excisional surgery was limited strictly to life-threatening situations, absolute nonresponse to drug treatment, and severe intervisceral fistulae. The operated patients (N = 93) had a lower relapse rate than the patients treated conservatively (N = 112), 20% and 51%, respectively, after four years. There were considerably fewer relapses in Crohn's colitis patients who were operated upon than in conservatively treated patients (18% versus 67% after four years); the same was found for ileocolitis (20% vs 49% after four years), but there was no difference between the treatment groups in ileitis (25-30% relapses for both after four years). In addition the patients with Crohn's disease of the colon had a more favorable course after resection with respect to symptoms, clinical and laboratory findings, and CDAI in remission. This paper gives data only for surgery in severe clinical situations and does not give a rationale for earlier surgery. This problem should now be studied in a randomized trial.

Adult↗
PubMed1989

Differential effects of acute mental stress on interdigestive secretion of gastric acid, pancreatic enzymes, and gastroduodenal motility.

To study the effects of acute mental stress on gastric and pancreatic secretion, 12 healthy fasting volunteers swallowed two multilumen tubes, which allowed continuous aspiration of gastric and duodenal juices and measurement of motility of the stomach and the duodenum. In each study at least three duodenal phase III complexes of the migrating motor complex were recorded. In randomized order after the first or second duodenal phase III, mental stress was induced for 60 min by means of solving anagrams and doing mental arithmetic. Mental stress significantly increased the duration of the migrating motor complex by 60% (137.9 +/- 16.3 vs 86.1 +/- 13.0). Gastric flow rate and gastric acid output were not significantly altered. Duodenal flow rate was not changed during the stress period but significantly decreased by more than 52% in the following 30-min resting period. Duodenal concentration and output of chymotrypsin were significantly increased during the second 30-min period of acute mental stress; chymotrypsin output was significantly reduced in the poststress period. We conclude that acute mental stress has different effects on the stomach, the pancreas, and the upper gastrointestinal motility. The mechanisms by which the central nervous activity induced by mental stress affects the motility and secretion of the upper gastrointestinal tract remain to be elucidated.

Adult↗
PubMed1989

The effect of a new synthetic cholinergic compound (aclatonium napadisilate) on interdigestive motility and pancreatic function in humans.

To investigate the effect of aclatonium napadisilate (Ac), a synthetic cholinergic compound, on human interdigestive gastrointestinal function, six healthy volunteers underwent gastrointestinal intubation for measurement of duodeno-jejunal motor activity and pancreatic enzyme secretion. Each subject was studied twice on two separate days and received either aclatonium (300 mg) or placebo intraduodenally in randomized order. Aclatonium significantly increased the overall length of the cycle of interdigestive motor complex (IMC) by a mean of 34% (p less than 0.05) without stimulating the phases of increased motor activity. Aclatonium slightly, but significantly increased output of lipase during phase II of the IMC (p less than 0.05), whereas outputs during phase I and III were not significantly changed. We conclude that aclatonium in a dose of 300 mg has only weak cholinergic effects on motility and exocrine pancreatic secretion in healthy humans during the interdigestive state.

Acetylcholine↗
PubMed1989

Effect of neural blockade on somatostatin-induced inhibition of exocrine pancreatic secretion.

In vivo somatostatin inhibits exocrine pancreatic secretion. In in vitro experiments, such as the isolated perfused pancreas, somatostatin fails to inhibit exocrine pancreatic secretion. This suggests an indirect action of somatostatin, such as modulation of neural regulation. In the anesthetized rat we tested the inhibitory capacity of somatostatin in the presence of neural blockade in vivo. Neither the drugs given intravenously--phentolamine, propranolol, atropine and naloxone--nor vagotomy were able to prevent somatostatin-induced inhibition of exocrine pancreatic secretion. We conclude that somatostatin-induced inhibition of exocrine pancreatic secretion is not dependent on intact extrinsic innervation.

Animals↗
PubMed1989

Rioprostil, a new prostaglandin E1, prevents cyclosporin A-induced damage to endocrine and exocrine pancreas.

The possibility that rioprostil can prevent cyclosporin A-induced damage to the pancreas is investigated. Cyclosporin A is given to rats once daily intragastrically in doses of 5, 10 and 20 mg/kg body weight. These doses cause dose dependent significant reduction of insulin release and enzyme secretion from the arterially perfused isolated pancreas. The subcutaneous injection of rioprostil, 15 micrograms/kg twice daily, could completely prevent the effects of 5 mg/kg cyclosporin A on insulin release and could completely prevent the effects of 5 mg/kg cyclosporin A on insulin release and could completely prevent the effects of 5 mg/kg cyclosporin A on insulin release and could also afford significant protection from the effects of 10 and 20 mg/kg cyclosporin A on both insulin release and enzyme secretion. The cytoprotective action of rioprostil on the pancreas may have therapeutic implications.

Animals↗
PubMed1989

[Recurrent gastroparesis following abdominal irradiation. Therapy with cisapride].

Following abdominal radiation a 16-year-old male patient developed nausea and vomiting secondary to gastric stasis, dilatation and impairment of antral motility. Symptoms improved after 2 months of treatment with a cholinergic agonist. Now, 7 years later, symptoms recurred. Cisapride, a newly developed agent which stimulates gastrointestinal motility probably evoked a prompt increase of antral motility and gastric emptying. We conclude that abdominal irradiation may cause gastrointestinal motility disturbances which may respond to medical therapy.

Adolescent↗
PubMed1989

Pancreatic secretory response to intravenous caerulein and intraduodenal tryptophan studies: before and after stepwise removal of the extrinsic nerves of the pancreas in dogs.

In two sets of 6 dogs with gastric and pancreatic fistulas, we studied the effect of atropine (14 nmol/kg.h i.v.) on the pancreatic secretory response to intravenous caerulein and to intraduodenal perfusion with tryptophan (both given with a secretin background) before and after stepwise removal of the extrinsic nerves of the pancreas, i.e., celiac and superior mesenteric ganglionectomy alone or truncal vagotomy alone and truncal vagotomy plus celiac and superior mesenteric ganglionectomy. Atropine significantly (p less than 0.05) depressed the protein output in the basal state and in response to secretin at each stage of innervation. The incremental protein response to caerulein was not altered by the various denervation operations nor by atropine. Truncal vagotomy alone significantly decreased the incremental protein response to low (0.12, 0.37, and 1.1 mmol/h) but not high loads of tryptophan. Ganglionectomy in combination with vagotomy did not further depress the incremental protein response to low loads of tryptophan. Atropine significantly reduced the incremental protein response to low loads of tryptophan only in intact innervated animals. Ganglionectomy alone did not alter the incremental protein response to any load of tryptophan. Ganglionectomy, truncal vagotomy, and atropine did not alter basal or tryptophan-stimulated levels of plasma cholecystokininlike immunoreactivity. We conclude that (a) neither the extrinsic nor the intrinsic cholinergic pancreatic nerves modulate the protein response to caerulein; (b) the sympathetic pancreatic nerves do not mediate the response to tryptophan; (c) the protein response to intraduodenal tryptophan is at least in part mediated by long, cholinergic, enteropancreatic reflexes with both afferent and efferent fibers running within the vagus nerves; and (d) release of cholecystokinin by intestinal tryptophan is not under cholinergic or splanchnic control.

Animals↗
PubMed1988

An amino-terminal fragment of cholecystokinin-58 is present in the gut: evidence for a similar processing site of procholecystokinin in canine gut and brain.

Radioimmunoassays using antibodies specific for the carboxyl terminus of cholecystokinin (CCK) and the midportion of CCK-58 (raised against synthetic canine CCK-33-(1-27] revealed the existence of a CCK fragment in canine gut and brain extracts which lacks the biologically active carboxyl terminal immunoreactivity. This material eluted on Sephadex G-50 gel permeation chromatography in the region of CCK-58, on high-pressure liquid chromatography (HPLC) after CCK-39 and before CCK-58, and on cation-exchange FPLC it eluted after CCK-58. The immunoreactive pattern, the ratio of absorbance at 280-220 nm and the chromatographic elution positions suggest that this large CCK-like molecule represents an amino-terminal fragment of CCK-58. This fragment is present in canine gut and brain. Therefore, a similar processing site of procholecystokinin is suggested in both tissues.

Animals↗