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Biomedical subjects

G E Feurle

Publications and source records attributed to G E Feurle.

At least 19 recordsLinked to original sources
PubMed1992

Identification of xenin, a xenopsin-related peptide, in the human gastric mucosa and its effect on exocrine pancreatic secretion.

One of the peptides previously discovered in amphibians is the octapeptide xenopsin. As immunohistochemistry has also indicated the presence of xenopsin immunoreactivity in man, we extracted in the present investigation xenopsin-immunoreactive material from human gastric mucosa and purified it to homogeneity with several high performance liquid chromatography (HPLC) reverse phase and ion exchange chromatographic steps. The eluates were monitored with a radioimmunoassay for amphibian xenopsin. Determination of the amino acid sequence revealed a 25-amino acid peptide having 6 C-terminal amino acids in common with amphibian xenopsin. The sequence of this peptide, termed xenin 25, is M-L-T-K-F-E-T-K-S-A-R-V-K-G-L-S-F-H-P-K-R-P-W-I-L. The peptide was custom-synthesized. Mass spectrometry of the synthetic and the extracted peptide revealed identical molecular mass. Purification of 250 ml of human postprandial plasma with Sep-Pak C18 cartridges, reverse phase HPLC, and ion exchange chromatography demonstrated circulating xenin immunoreactivity at a retention time identical to xenin 25. The amount of xenin immunoreactivity at the position of xenin 25 on C18-HPLC increased significantly after a meal. A radioimmunoassay utilizing antibodies to xenin 25 and a 125I-labeled analogue of xenin 25 was used to measure immunoreactive xenin in the plasma of 10 volunteers. There was a significant rise of xenin immunoreactivity in the plasma after a meal. Intravenous infusion of the synthetic peptide in dogs stimulated exocrine pancreatic secretion beginning at a dose of 4 pmol/kg/min. The maximal effect was seen with 64 pmol/kg/min. We have detected, therefore, a new peptide, xenin 25, in human gastric mucosa; we have provided evidence for the presence of this peptide in the human circulation, and have shown a rise of plasma xenin concentrations after a meal. This peptide stimulates exocrine pancreatic secretion. Its physiologic role deserves further investigation.

Amino Acid Sequence↗
PubMed1991

The site of action of neurotensin in the rat pancreas.

The tridecapeptide neurotensin, present in endocrine cells of the ileal mucosa and in nerve bodies of cerebral nuclei, may play a role in the physiology of exocrine pancreatic regulation. This assumption is based on two observations: Neurotensin appears in the blood stream after a fatty meal and neurotensin stimulates exocrine pancreatic secretion. There has, however, been controversy on the site of action of this peptide since some investigators did not observe an effect on the pancreas in vitro and suggested, therefore, an indirect, perhaps neural or even central site of action. In the present investigation, we compared the action of neurotensin on the exocrine pancreas in vivo in the anesthetized rat after intracerebroventricular (i.c.v.) injection and after i.v. infusion and in vitro after incubation of the pancreas in three different preparations: isolated dispersed acini, isolated lobuli, and isolated total pancreas. We found that i.c.v. application of neurotensin stimulated exocrine pancreatic secretion only when doses were applied that led to elevated peripheral plasma neurotensin levels. In vitro, the action of neurotensin was very weak and the optimal dose was integrity dependent; e.g., a concentration of 10(-4) and 10(-5) M neurotensin was necessary to stimulate amylase release from isolated acini, 10(-8) M neurotensin induced amylase release from isolates lobuli, and 10(-9) M neurotensin released amylase from the intact pancreas. Intravenously, neurotensin resulted in a greater amylase release over basal than in any of the in vitro experiments. We conclude that neurotensin acts directly on the pancreatic acini but that the sensitivity of the pancreas is greatly enhanced when the organ is intact and has normal neural and vascular communications.(ABSTRACT TRUNCATED AT 250 WORDS)

Amylases↗
PubMed1991

Acute small bowel ischemia without transmural infarction.

Two patients with atrial fibrillation had abrupt onset of abdominal pain and massive small bowel distension suggesting mesenterial artery embolism. One patient had dilation of the left atrium and ventricle, the other a mitral value prolapse syndrome with a dilated left atrium. Both patients were treated conservatively and gradually recovered. A small bowel series performed several weeks after the acute episode showed loss of normal mucosa and narrowing of a long segment of the small bowel. A control examination in one patient one year later, still revealed jejunal mucosal abnormalities and stenosis, features similar to those occurring in Crohn's disease. Our observations suggest that analogous to ischemic colitis, an entity of acute ischemic small bowel enteritis exists. Mesenteric ischemia apparently can induce a clinical syndrome of "regional enteritis". The radiologic features should not be confused with those of Crohn's disease.

Aged↗
PubMed1990

Distinct immunohistochemical findings in columnar epithelium of esophageal inlet patch and of Barrett's esophagus.

Immunohistochemistry was performed on biopsies of columnar mucosa from 11 patients with Barrett's esophagus and 11 patients with columnar mucosa in the cranial esophagus, the "inlet patch." Both epithelia contained endocrine cells, immunoreactive to antisera against serotonin, glucagon, somatostatin, and pancreatic polypeptide; the specialized mucosa of Barrett's esophagus contained, in addition, neurotensin-immunoreactive cells, and in the mucosa of an inlet patch we found a gastrin cell. These findings are not compatible with some of the current theories on the origin of these epithelia. The mucosa of the inlet patch has been considered to consist of heterotopic gastric mucosa. The mucosa of the adult human stomach, however, does not contain glucagon cells. These cells are only present in the early embryonic stomach, and they disappear during embryonogenesis. According to our findings, the mucosa of the inlet patch therefore represents embryonic gastric mucosa. The specialized columnar epithelium of Barrett's esophagus has been considered to have evolved from gastric mucous neck cells. However, although glucagon cells are a feature of the embryonic stomach, neurotensin-immunoreactive cells have not been found in the gastric mucosa. Our study suggests that the specialized columnar epithelium of Barrett's esophagus originates from a very immature multipotent gastrointestinal stem cell.

Aged↗
PubMed1990

Dissimilar trophic effects of cerulein and xenopsin on the rat pancreas.

Cholecystokinin (CCK), gastrin, cerulein, and other analogs are known to stimulate the growth of the rat pancreas. In the present study, we compared the trophic action of a member of this gastrin/CCK family, the amphibian peptide cerulein, with a member of the structurally unrelated neurotensin/xenopsin group, the amphibian peptide xenopsin. For this purpose, 0.56 nmols/kg cerulein, 1.0 nmols/kg xenopsin, or normal saline were injected intraperitoneally three times a day in 28 rats for 3 d. Pancreatic weight, DNA, and incorporation of 3H-thymidine into DNA were determined. In another study, pancreatic weight, DNA, and the polyamines, putrescine, spermidine, and spermine, were determined after a single dose of 2.7 nmol/kg cerulein, 4.5 nmol/kg xenopsin, or saline. The polyamines were measured by reverse-phase HPLC and post-column derivatization. Cerulein increased pancreatic weight, stimulated 3H-thymidine incorporation into DNA, and raised putrescine concentrations significantly, but led to a significant reduction of pancreatic DNA concentration. Xenopsin also stimulated 3H-thymidine incorporation into DNA, but did not affect pancreatic weight, DNA concentration, or the polyamines during the 4 h of the experiment. These findings suggest that cerulein, in the dose and intervals applied, initiated hyperplasia and induced hypertrophy of the pancreas, whereas xenopsin only initiated hyperplasia. These results, together with the dissimilar secretory effects of the two peptide families, may be the expression of a dissimilar mode of action. However, it cannot be excluded that, since cerulein is more potent than xenopsin, the differences also are owing to dosage. We conclude that cerulein and xenopsin, which both have trophic effects on the pancreas, may act by different mechanisms.

Animals↗
PubMed1990

Arteriovenous shunting and cholestasis in hepatic hemangiomatosis associated with metoclopramide.

Diffuse hemangiomatosis of the liver became apparent in a 22-year-old woman while she was receiving medication with metoclopramide and experiencing the well-known adverse effect of the drug, hyperprolactinemia with secondary amenorrhea and galactorrhea. The hemangiomatosis was demonstrated by ultrasonography, computerized tomography, arteriography, and laparotomy with biopsy. When arteriovenous shunting became life-threatening and severe abdominal pain and cholestasis developed, the patient's name was placed on the waiting list for liver transplantation. However, after stopping the medication with metoclopramide, abdominal pain disappeared, cholestasis decreased, and the arteriovenous shunts in the liver closed completely. This course of disease represents either a spontaneous or a drug-induced activation and regression of hepatic hemangiomatosis. However, the long-term metoclopramide medication indicates a potential role of this drug in the promotion of hepatic angiogenesis. Hepatic angiomatosis in the adult seems to be neither a static nor a steadily progressive disorder but a process with active and regressive phases probably induced by a transient imbalance of angiogenic and angiostatic factors. Such a course should be kept in mind when major surgery or liver transplantation for hepatic hemangiomatosis is planned. It seems prudent to obtain a thorough drug history of all patients with hepatic hemangiomatosis. Whether hepatic hemangiomatosis can be drug induced or not, further investigation of the factors involved in hepatic angiogenesis is warranted.

Adult↗
PubMed1990

Morphometry and function of islet cells after different forms of drainage at pancreatic transplantation in rats.

The survival of endocrine cells of the islets is crucial for a successful transplantation of the pancreas in the treatment of diabetes mellitus. In the present investigation, we compared the effect of four techniques of whole pancreas transplantation in rats on the endocrine cells of islets of Langerhans. Impairment of the endocrine function of the pancreas with a decrease in the k value was seen after 6 months in the group with duct ligation, and after 12 months in the groups with latex and ethibloc occlusion. An open pancreatic duct maintains a more stable endocrine function than in duct-ligated or occluded grafts. Fasting plasma insulin and somatostatin were elevated in transplanted rats. Whichever method of transplantation we chose, the cell ratio remained unchanged compared with the control group, even after 12 months. Therefore, only intact islet architecture enables a normal endocrine pancreatic function.

Animals↗
PubMed1989

Cholecystokinin influences pancreatic trophism following total gastrectomy in rats.

In rats, total gastrectomy (TG) has been shown to induce pancreatic hyperplasia and increased tissue concentrations of pancreatic trypsin and amylase, whereas lipase concentration was decreased. We performed total gastrectomy with the additional insertion of a duodenal tube in 17 rats. A central venous catheter was placed after 3 wk. The control groups consisted of sham-operated rats with a gastrotomy plus duodenal tube and a group of rats with only a duodenal tube. The rats received meal stimulation with a 6 mL liquid diet (3 mL oil, 2 mL amino acid solution, and 1 mL glucose) via duodenal tube upon recuperation. Blood samples were taken before as well as 5, 15, 30, and 60 minutes after the meal and analyzed for insulin, pancreatic glucagon, gastrin, and CCK by specific RIA techniques. Glucose tolerance was found to be impaired after total gastrectomy. Though insulin release was delayed compared to the controls, the integrated postprandial output was unchanged. The pancreatic glucagon release after the meal increased 83% in TG rats, compared to control rats. The baseline and postprandial gastrin values diminished 70% compared to control animals. Neither group exhibited a postprandial increase in gastrin levels. TG led to an increased postprandial CCK output of 72% compared to controls. The trophic changes of rat exocrine pancreas following total gastrectomy, therefore, could be based on an elevated postprandial release of CCK.

Animals↗
PubMed1989

Olsalazine versus placebo in the treatment of mild to moderate ulcerative colitis: a randomised double blind trial.

The effect of olsalazine, an analogue of sulphasalazine, consisting of two molecules 5-aminosalicylic acid linked by an azobond has been investigated for the treatment of ulcerative colitis. In a randomised double blind trial we compared 2 g olsalazine with placebo for four weeks. Of the 105 patients, with mild to moderate ulcerative colitis, entered in the trial 52 received olsalazine, and 53 placebo. Treatment had to be terminated prematurely because of untoward effects of olsalazine (mainly diarrhoea) in three patients and treatment failure--that is, increased rectal bleeding in four patients (olsalazine group: one placebo group: three). After four weeks' treatment, a statistically significant improvement in the endoscopic findings in rectum and a positive trend in the reduction of rectal mucus and blood discharge was observed in the patients treated with olsalazine. No statistically significant difference was found for other factors, including stool frequency, consistency, urge to defecate, abdominal pain, and biopsy findings. A comparison between these clinical and endoscopic parameters at study entry and those at study completion (within drug evaluation) showed significant improvement in six of 10 parameters during treatment with olsalazine and in two of 10 during placebo treatment. This difference suggests the significant effect of olsalazine. We conclude that 2 g olsalazine was tolerated as well as placebo, apart from causing diarrhoea in some patients and was slightly superior to placebo during four weeks' treatment of mild to moderate ulcerative colitis. A study with 3 or 4 g olsalazine per day may show a more definite effect.

Adolescent↗
PubMed1988

G-cell hyperplasia in rats with pyloric stenosis.

Since little is known about the pathophysiology of pyloric stenosis, we created a partial gastric outlet obstruction in 13 Wistar rats by placing a nonabsorbable ligature of defined size around the pylorus. Sham operations were performed in 10 rats. The animals from both groups were killed after four months. G-cell count and gastrin content were determined in 10 parallel strips, which were cut by razor blades mounted on a handle. Gastric size and weight as well as thickness of mucosal and muscular layers and serum gastrin concentration were also determined. Body weight of the animals with pyloric stenosis was lower and gastric weight higher than that of the controls. Furthermore, we found an enlarged G-cell area and G-cell hyperplasia, an increased surface area and thickness of the mucosal and muscular layers of the stomach, and in the majority of rats, elevated serum gastrin levels. Total G-cell count was 583,720 +/- 90,561 in the rats with pyloric stenosis and 385,775 +/- 15,820 (mean +/- SEM) in the control rats (P less than 0.04). We conclude that partial gastric outlet obstruction in rats leads to G-cell hyperplasia and that this experiment may serve as a model for pyloric stenosis in man.

Animals↗
PubMed1988

Immunocytochemical evidence for the colocalization of neurotensin/xenopsin- and gastrin/caerulein-immunoreactive substances in Xenopus laevis gastrointestinal tract.

Distribution and association of neurotensin (NT)- and xenopsin (XP)-like peptides were investigated using immunocytochemical techniques in the amphibian gut. Antisera against both groups of peptides showed an identical distribution pattern of NT- and XP-positive cells in Xenopus laevis gastrointestinal tract. Immunolabeling of consecutive semithin sections revealed the coexistence of NT- and XP-like substances within cells of the stomach and small intestine. Recent reports of the colocalization of XP-like material with gastrin in mammalian G cells led us to study the association of NT/XP-like peptides with members of the gastrin/cholecystokinin (CCK)/caerulein (G/C) family in amphibians. The data obtained from immunolabeling serial sections with NT/XP-specific and G/C-specific antisera show that in some intestine NT/XP- and G/C-like peptides do exist in the same cells. In the stomach, however, G/C-like material is confined to endocrine cells of the antral region, while NT/XP-like substances occur in distinct cells accumulating in cardial glands but absent in the pyloric glands. Our findings thus indicate that in amphibian gastrointestinal tract there is some association between the regulatory peptide families NT/XP and G/C, similar to mammals. The regional distribution of both hormone families, however, is different from that in mammals.

Animals↗
PubMed1988

Pancreatic trophism following colectomy in rats: the potential role of gastrointestinal hormones.

It has been shown that the large bowel contains substances with a potential to inhibit exocrine pancreatic function. Following large bowel removal in rats, there is an increase of pancreatic weight, digestive enzyme concentration, and secretion capacity in vitro. To evaluate the role of various GI hormones in the exocrine pancreatic adaptation following colectomy, we measured plasma cholecystokinin (CCK), neurotensin, glucagon, and insulin after meal stimulation. The test meal was applied via a transabdominal gastric tube in eight colectomized Wistar rats after a median of 18 days following surgery. Ten rats with a gastric tube without previous bowel surgery served as controls. After large bowel removal, there was impaired glucose tolerance and attenuated plasma insulin secretion. Baseline plasma glucagon levels were increased after colon removal, whereas the total postprandial glucagon release was decreased. Baseline and postprandial neurotensin values were comparable in both the experimental and control animals. Baseline and postprandial CCK plasma levels were intensely increased in the colectomized rats. It is assumed that the baseline and postprandial CCK pattern in rats after subtotal colectomy is responsible for exocrine pancreatic adaptation.

Animals↗
PubMed1988

Loss of predictive value of gastric ulcer symptoms in a randomized treatment trial.

Analysis of clinical data obtained in a double-blind randomized study, which compared liquid antacid (neutralizing capacity 120 mmol per day) with 1 g cimetidine in the treatment of 125 patients with gastric ulcer, revealed that, before starting treatment, 71% of the patients complained of epigastric pain, approximately 50% of bloating, and approximately 30% of nausea, heartburn, constipation or vomiting. Epigastric pain before treatment was significantly more frequent in patients with large ulcers (P less than 0.05) and in patients with ulcers unhealed after 4 weeks of therapy (P less than 0.05). This finding was the result of a highly significant correlation between diurnal epigastric pain and ulcer size and delayed healing (P less than 0.005). Nocturnal pain did not correlate with prognosis. In contrast to this correlation between pain before therapy and healing, the disappearance of epigastric pain with therapy did not signify ulcer healing. Only 14 (38%) of the 37 patients with healed ulcer were free from pain after the 4 weeks of therapy, whereas 25 (49%) of the 52 patients with persistent ulcers had no pain at this time. Placebo pain tablets relieved ulcer pain effectively in more than 85% of the patients, irrespective of whether the ulcer was healing or not. The other symptoms (bloating, nausea, heartburn, constipation or vomiting) were also alleviated by 4 weeks of therapy but no correlation was found with ulcer size or prognosis. The loss of the prognostic significance of ulcer pain is probably due to a complex interaction of the trial schedule on the patient's level of consciousness.(ABSTRACT TRUNCATED AT 250 WORDS)

Antacids↗