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V Eysselein

Publications and source records attributed to V Eysselein.

16 recordsLinked to original sources
PubMed1998

Colonic stents in colorectal obstruction.

Obstruction is the presenting symptom of colorectal cancer in up to 40 per cent of patients. Benign strictures and other neoplasms including lymphoma and gynecologic tumors occur as well. Emergent operative therapy is often suboptimal and associated with significant morbidity and mortality. Our objective was to review our experience with stent placement for colonic obstruction. Seven patients underwent stent placement for a total of eight procedures. There were three patients with unresectable colorectal cancer, two patients with metastatic gynecologic cancer, one patient with rectal lymphoma, and one patient with metastatic cancer of unknown primary. All colonic stents were Wallstents placed by the same endoscopist under fluoroscopic and endoscopic guidance. Stents were successfully placed in all patients without complication. One patient underwent placement of two stents in succession for a long stenosis. Six of seven patients (86%) had resolution of the obstruction and return of bowel function. Five of seven were tolerating a diet within 24 hours. One patient's mental status did not allow for oral intake. Four patients were discharged within 48 hours. Two patients died within the same hospitalization as a result of metastatic disease. One patient was found to have multilevel disease requiring stoma placement. There was no morbidity or mortality associated with stent placement, and 86 per cent of patients had palliation of the obstruction. We conclude that colonic stent placement is a safe and effective therapy for colorectal obstruction at this institution.

Colorectal Neoplasms↗
PubMed1994

Protective function of extrinsic sensory neurons in acute rabbit experimental colitis.

BACKGROUND/AIMS: Sensory nerves appear to have a protective effect against acute injury in the gastric mucosa. Their function in the intestine is unclear. METHODS: In this study an immune-complex model of colitis was used to induce inflammation in the distal colon with and without functional ablation of sensory neurons by capsaicin pretreatment. RESULTS: Colitis was more severe in the capsaicin-pretreated group than in the vehicle group 48 and 96 hours after induction of colitis. Neutrophil infiltration, expressed as inflammatory index, was significantly increased to 4.25 +/- 0.4 vs. 1.83 +/- 0.5 at 48 hours and to 2.66 +/- 0.6 vs. 1.65 +/- 0.3 at 96 hours in the capsaicin group and the vehicle group, respectively. The microscopic ulcer index also was significantly increased in the capsaicin-pretreated group compared with the vehicle group (63.3 +/- 10.6 vs. 3.3 +/- 2.4 at 48 hours, 20.0 +/- 8.4 vs. 1.5 +/- 1.1 at 96 hours). Immunoreactive substance P (SP) and calcitonin gene-related peptide (CGRP) contents were decreased in extracts of inflamed compared with uninflamed colon. CONCLUSIONS: These data suggest that sensory neurons have a protective role in an acute rabbit model of experimental colitis by release of sensory neuropeptides (SP, CGRP), which may modulate vascular tone and mucosal blood flow.

Animals↗
PubMed1993

Hereditary error in epidermal growth factor prohormone metabolism in a rat model of autosomal dominant polycystic kidney disease.

Normal Sprague Dawley (SPRD) rats of both sexes secrete an 165 kDa EGF prohormone in urine. Sexually mature Hannover-Sprague Dawley rats (Han:SPRD) heterozygous males and females with autosomal dominant polycystic kidney disease (ADPKD) secrete a prohormone of similar molecular mass in urine. The male, but not the female, also secretes two variant prohormone isoforms with molecular masses close to 200 kDa. Both the 165 and 200 kDa EGF prohormone isoforms are totally absent, in urine, at 11 months of age in male but not in female heterozygous Han:SPRD rats. At this age, the male kidneys exhibit numerous cysts filled with colorless fluids and these fluids contain abundant quantities of a 66 kDa EGF prohormone metabolite. Homozygous Han:SPRD rats which are born with cystic disease secrete only trace amounts of 165 kDa EGF prohormone in their urine while their normal looking littermates secrete the 165 kDa EGF prohormone in abundant quantities. The cyst fluids of homozygous rats contain trace amounts of 165 and 154 kDa EGF prohormone isoforms while the 66 kDa EGF prohormone metabolites present in abundant quantities. The massive amounts of 66 kDa EGF prohormone metabolite in cyst fluids of PKD rats suggests that EGF prohormone and its isoforms undergo aberrant proteolysis in association with cyst pathogenesis both in heterozygous and homozygous kidneys. The specific retention of the 66 kDa EGF prohormone metabolite within the cyst suggests that this molecule may function as a cystogen.

Animals↗
PubMed1991

Characterization of canine intestinal cholecystokinin-58 lacking its carboxyl-terminal nonapeptide. Evidence for similar post-translational processing in brain and gut.

An antibody raised against a synthetic cholecystokinin (CCK) analog, (1-27)-(CCK)-33, corresponding to the midregion of CCK-58, detected immunoreactivity in intestinal extracts which eluted between the positions of CCK-33/39 and CCK-58 on high performance liquid chromatography. This peak, lacking carboxyl-terminal cholecystokinin immunoreactivity, was purified by reverse phase and cation-exchange chromatographies. Amino acid, mass spectral, and microsequence analysis established that it was the amino-terminal desnonapeptide fragment of cholecystokinin-58, (1-49)-CCK-58. It was demonstrated further that CCK-58 has less biological activity than CCK-8, suggesting that the amino terminus either sterically hindered the ability of CCK-58 to exert its biological activity or that its amino terminus acted at another site to inhibit release of amylase from rat pancreatic acini. The desnonapeptide of CCK-58 by itself had no biological activity, nor did it affect CCK-8-stimulated amylase release from isolated rat pancreatic acini, suggesting that the amino terminus shields the carboxyl terminus from expressing its biological activity. Its presence in intestine suggests that it is released into the circulation where it could be detected by midregion antibodies. The presence of high proportions of (1-49)-CCK-58 indicates that most CCK-8 is directly derived from CCK-58. Its occurrence in brain and intestine indicates similar processing for procholecystokinin in both tissues.

Amino Acid Sequence↗
PubMed1990

Substance P and CGRP mediate motor response of rabbit colon to capsaicin.

Primary afferent nerve terminals located in the mammalian gut wall may play a role in region-specific modulation of gastrointestinal motility. In the present study, we sought to characterize the effect of neuropeptides released from these afferents by capsaicin (CAP) on contractile activity of smooth muscle from the distal rabbit colon. CAP caused a release of acetylcholine and immunoreactivity for substance P (SP) and calcitonin gene-related peptide (CGRP) from the muscle coat. CAP caused a dose-dependent transient stimulation of longitudinal muscle contractions, followed by prolonged inhibition of spontaneous but not stimulated contractile activity. The initial stimulation was abolished by the SP antagonist spantide and by atropine. The inhibitory effect was reduced by repeated exposure of muscle to CGRP. The effect of CGRP on spontaneous contractions differed between longitudinal and circular muscle. In longitudinal muscle, a stimulation was preceded by a transient inhibition, whereas in circular muscle, only inhibition was seen. Both effects were resistant to tetrodotoxin. Repeated exposure of circular but not longitudinal muscle to CGRP resulted in a disappearance of the peptide's inhibitory effect. Exogenously applied CGRP was only a weak antagonist of contractions stimulated by SP and bethanechol. These findings suggest that in the rabbit colon at least the following two neuropeptides are released from CAP-sensitive nerve fibers: a neurokinin peptide from nerve terminals located within the myenteric plexus and CGRP from terminals probably located within the circular muscle layer.

Acetylcholine↗
PubMed1987

Gastrin is not a physiological regulator of pancreatic exocrine secretion in the dog.

The role of gastrin as a regulator of exocrine pancreatic secretion has not been proven adequately. In the present study we therefore compared the relative molar potencies of sulfated and unsulfated gastrin 17 with structurally related CCK peptides (synthetic CCK-8 and natural porcine CCK-33) in stimulating exocrine pancreatic secretion in conscious dogs. Dose response curves were constructed for pancreatic and gastric acid secretion. Plasma gastrin levels after exogenous gastrin 17-I and -II were compared with postprandial gastrin concentrations (meal: ground beef 20 g/kg body wt). The molar potency estimates calculated with synthetic CCK8 as standard (potency = 1.00) for pancreatic protein secretion were natural porcine 50% pure CCK-33 1.60, gastrin 17-I 0.12, and gastrin 17-II 0.16. All four peptides induced a dose-dependent increase in pancreatic bicarbonate output. However, the blood concentrations needed to stimulate pancreatic secretion were above the postprandial gastrin levels. Our data indicate that both gastrin 17 peptides are not physiological regulators of pancreatic enzyme secretion in dogs.

Animals↗
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↗
PubMed1986

New molecular forms of cholecystokinin. Microsequence analysis of forms previously characterized by chromatographic methods.

Cholecystokinin previously has been characterized by chromatographic and immunological techniques. Analysis of cDNA has revealed the structure of preprocholecystokinin. The predicted processing sites of preprocholecystokinin cannot account for the multiple forms of cholecystokinin detected. This report details the isolation and characterization of cholecystokinin peptides containing 58, 39, 33, 25, 18, 8, 7, and 5 amino acids. None of the cleavages that occurred to form these peptides was at the carboxyl side of double basic residues. Cholecystokinin 25, 18, and 7 have not previously been isolated and identified by sequence analysis. The processing that forms these peptides includes cleavage after single basic residues for the 58, 39, 33, and 8 amino acid peptides. The 25, 18, 7, and 5 amino acid peptides must be formed by other endopeptidases or combinations of endo- and exopeptidases. The analysis of this series of peptides provides the chemical basis for structural differences in cholecystokinin molecules previously demonstrated by chromatographic and immunological methods. These structures provide insight into tissue-specific processing that occurs for this important regulatory peptide in intestine and brain.

Amino Acid Sequence↗
PubMed1986

Clinical and biochemical aspects of the insulin autoimmune syndrome (IAIS).

A 44-year old patient presented with recurrent hypoglycemic attacks after ingestion of carbohydrates. High insulin levels in the range of 350 microU/ml (normal range less than 20 microU/ml) were detected which rose to peak levels of 2,460 microU/ml (normal range less than 300 microU/ml) after oral glucose. The apparently high insulin concentrations were caused by insulin autoantibodies interfering in the radioimmunoassay (RIA) system (and thus with correct insulin quantitation). 125I-insulin added to the patient's serum was not bound to dextran-coated charcoal but was precipitated with antihuman IgG serum. The antibodies bound human, porcine, and bovine insulin with similar affinity. Following Sephadex G-50 gel filtration, the patient's insulin eluted after the void volume. Free insulin was extracted from serum using Sep-Pak C 18 cartridges and characterized by high pressure liquid chromatography (HPLC); it eluted similarly to synthetic human insulin. Quantitation of free insulin during a hypoglycemic attack (3.5 h after oral glucose, with a blood sugar of 20 mg/dl) showed an increased insulin level of 50 microU/ml. Insulin receptor concentration on erythrocytes was near the lower normal limit. We believe that the insulin antibodies present in this patient's serum (who supposedly never received insulin) led to the formation of a large circulating insulin pool, binding the insulin released after glucose stimulation, and causing hypoglycemias by delayed postprandial liberation of bound insulin.

Adult↗
PubMed1986

Action of intravenous ethanol and atropine on the secretion of gastric acid, pancreatic enzymes, and bile acids and the motility of the upper gastrointestinal tract in nonalcoholic humans.

To investigate the influence of the cholinergic nerves on the action of i.v. ethanol on interdigestive gastric acid, pancreatic enzyme, and bile acid output, seven healthy volunteers were studied. On each of 4 different days, they swallowed a multilumen intestinal tube system that allowed the measurement of intraluminal pressures and the collection of gastric and duodenal juice. The subjects received an i.v. infusion of either ethanol (600 mg/kg for 30 min followed by 3 mg/kg/min), atropine (5 mu/kg/h), a combination of both drugs, or NaCl. Whereas ethanol did not significantly influence motility, atropine induced motoric quiescence. Ethanol significantly (p less than 0.05) stimulated gastric acid output, by 55%, whereas atropine inhibited it by 91%. When ethanol and atropine were given together, gastric acid output was significantly higher than during atropine use alone. Both ethanol and atropine inhibited pancreatic amylase output--by 47% and by 82%, respectively. The degree of inhibition was 80% when ethanol and atropine were given simultaneously. Atropine but not ethanol significantly reduced bile acid output. The finding that atropine did not completely reverse the stimulating effect of i.v. ethanol on gastric acid secretion suggests that ethanol stimulates gastric acid secretion not only by a cholinergic but also by a noncholinergic mechanism. The observation that atropine did not reverse the inhibiting effect of ethanol suggests, but does not prove, that the effect of ethanol on the pancreas is predominantly mediated by cholinergic nerves.

Adult↗
PubMed1985

Different actions of intravenous ethanol on basal (= interdigestive) secretion of gastric acid, pancreatic enzymes and bile acids and gastrointestinal motility in man.

The action of an intravenous infusion of ethanol (10% v/v; given in a dose of 300 mg kg-1 body weight for 30 min followed by 3 mg kg-1 min-1 for 2 hr) on the basal (= interdigestive) gastrointestinal motor activity and the basal gastric acid, pancreatic amylase and bile acid secretion was determined in 6 healthy human volunteers. Ethanol did not affect the duration of the interdigestive motor complex and the output of bile acids into the duodenum. Ethanol significantly (P less than 0.05) stimulated the gastric acid output by about 2.2-fold and inhibited the pancreatic amylase output by about 43% as compared to control experiments in which an intravenous infusion of 0.15 M NaCl was given. Ethanol did not alter the mean plasma levels of gastrin and pancreatic polypeptide as compared to prestimulatory values and to control experiments. In conclusion, these results show that intravenous ethanol given in a moderate dose stimulates gastric acid output and inhibits pancreatic amylase output in fasting non-alcoholic human beings. The mechanism(s) of these different actions of ethanol is unknown since release of gastrin or pancreatic polypeptide by ethanol does not account for the observed effects of intravenous ethanol.

Adult↗
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↗