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Biomedical subjects

M V Singer

Publications and source records attributed to M V Singer.

At least 127 records · Page 7Linked to original sources
PubMed1990

[Paralytic ileus as an initial manifestation of malignant VIPoma of the pancreas--case report with review of the literature].

A 57-year old patient with a paralytic ileus of unknown origin was admitted to the intensive care unit. Because of the laboratory findings with therapy resistant hypokalemia, hypercalcemia and metabolic acidosis a VIPoma was suspected. Therapy with somatostatin resulted in correction of laboratory abnormalities and in normalization of gastrointestinal motility. Plasma concentrations of VIP and PP were elevated, ultrasonography revealed a pancreatic tumor. Postsurgical examination of the removal tumor tissue confirmed the diagnosis of a malignant VIPoma. Clinical symptoms, laboratory findings with and without somatostatin-therapy and immunhistochemical properties are described.

Biomarkers, Tumor↗
PubMed1990

[Effect of 1 week's administration of prednisone on gastric acid secretion and liberation of gastrin in healthy humans].

In a double-blind, randomized study we examined the effects of an oral administration of prednisone (60 mg/day for 6 days) or placebo on gastric acid output basally (BAO), in response to peptone meals 1%, 2%, 4% and 8%, 500 ml each) and to pentagastrin 6 micrograms/kg s.c. to determine maximal acid output, MAO) and on plasma gastrin levels in 14 healthy volunteers. Gastric acid output was measured by intragastric titration (pH 5.5). For gastrin determination we used a specific radioimmunoassay. Experiments were performed one day (day 0) before giving the drugs and one day (day 7) and one month (day 30) after finishing the treatment. Both groups were comparable in their gastric acid responses on day 0. Six days treatment with prednisone did not significantly alter BAO, MAO and the gastric acid response to peptone and pentagastrin. Also, one month after finishing the treatment there were no significant differences in gastric acid output. Both groups had similar plasma gastrin levels on each day. Prednisone did not significantly alter plasma gastrin levels. We conclude that a six-day treatment with prednisone does not alter BAO, MAO and gastric secretory responses to peptone nor release of gastrin in healthy human volunteers.

Administration, Oral↗
PubMed1990

[Absence of effect of atropine on exocrine pancreatic secretion stimulated by cerulein].

The effect of atropine, 0.9, 1.8, 7 and 29 nmol/kg-1/h-1, on pancreatic exocrine secretion has been measured in seven dogs with gastric and pancreatic fistula in response to IV administration of increasing doses of cerulein (3.7 to 118 pmol/kg-1/h-1). Secretin was perfused continuously, at a rate of 20.5 pmol/kg-1/h-1, starting one hour before perfusion of cerulein. The administration of atropine, 7 and 29 nmol/kg-1/h-1, significantly (p less than 0.05) decreased the protein response to secretin. Only the injection of 29 nmol/kg-1/h-1 of atropine produced a significant decrease in the secretion of bicarbonate in response to secretin. The administration of 3.7 pmol./kg-1/h-1 and larger doses of cerulein significantly increased the secretion of bicarbonate and protein, compared to the levels obtained with the administration of secretin alone. None of the atropine doses showed a significant effect on the pancreatic response to the administration of cerulein. Only the highest dose of atropine, 29 nmol/kg-1/h-1, modified cardiac rate. These findings are consistent with the hypothesis that cholinergic innervation does not modify the effect of cerulein, a CCK analogue, on the pancreatic secretion of protein and bicarbonate in the dog.

Animals↗
PubMed1990

[Effect of enalapril on heart rate, arterial blood pressure and exocrine pancreatic secretion in the alert dog].

A changed exocrine pancreatic secretion could be a pathogenetic factor of an acute pancreatitis after administration of angiotensin-converting enzyme (ace) inhibitors. In six conscious dogs with gastric and duodenal Thomas fistulas we studied the effect of an intravenous (iv.) bolus injection of 10 mg enalaprilat, an intraduodenal (id.) bolus injection of 20 and 40 mg enalapril (e.), and 0.15 M NaCl (20 ml iv., resp., id.) on pancreatic bicarbonate- and protein output in response to secretin (20.5 pmol/kg bw/h and caerulein (29.6 pmol/kg bw/h). Arterial blood pressure and heart rate we also measured. The iv. and id. injection of enalapril(at) significantly increased heart rate by 28% after 10 mg of e. iv. [peak 101 +/- 11 beats/min, N = 6, X +/- SEM] and by 13 resp. 37% after 20 resp. 40 mg e. id. [peak 89 +/- 4, resp., 108 +/- 7 beats/min] as compared to control [peak 79 +/- 5 beats/min]. Systolic blood pressure was significantly decreased by 6% after 10 mg e. iv. [lowest value 121 +/- 2 mm Hg] and by 8% and 9% after 20 and 40 mg e. id., respectively, [lowest value 119 +/- 2, resp., 118 +/- 1 mm Hg] as compared to control [lowest value 129 +/- 1 mm Hg]. The applied enalapril(at) doses had no significant effect on hormonal stimulated pancreatic bicarbonate- and protein output. The results confirmed the well known effects of enalapril(at) on heart rate and on arterial blood pressure. Beyond that the results exposed that therapeutical doses of enalapril(at) had no significant effect on exocrine pancreatic secretion. Conclusion of this study is that a pathogenetic role of pancreatic exocrine secretion in the ace-inhibitors and the acute pancreatitis induced by ace-inhibitors is unlikely.

Acid-Base Equilibrium↗
PubMed1990

Telenzepine, a new M1-receptor antagonist, is a more potent inhibitor of pentagastrin-stimulated gastric acid output than pirenzepine in dogs.

In conscious dogs with a gastric fistula we compared the action of different doses of telenzepine (ranging from 1 to 243 nmol/kg/h) and pirenzepine (ranging from 4.7 to 1170 nmol/kg/h) on gastric acid output in response to pentagastrin (1 to 8 micrograms/kg/h). Pentagastrin caused a dose-dependent increase in gastric acid output. A dose of 27 nmol/kg/h and all subsequent doses of telenzepine and a dose of 130 nmol/kg/h and all higher doses of pirenzepine significantly inhibited (up to 74% of control values) the gastric acid response to pentagastrin. Doses above 27 nmol/kg/h of telenzepine and doses above 130 nmol/kg/h of pirenzepine did not further inhibit the gastric acid output. Only the highest doses of telenzepine (243 nmol/kg/h) and pirenzepine (1170 nmol/kg/h) significantly increased heart rate from 66 +/- 3.1 to 77.1 +/- 3.9 and 72.5 +/- 3.2, respectively (beats/min, chi +/- SEM, n = 6). Differences between both drugs were not found with regard to cardiovascular responses of equipotent doses. We conclude that in conscious dogs with an intact stomach, the new M1-receptor antagonist telenzepine is, on a molar basis, more than 4.7 times more potent than pirenzepine in inhibiting pentagastrin-stimulated gastric acid output. This inhibition occurs at doses that do not increase heart rate, and, therefore, probably cause few systemic effects.

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

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

Effects of rioprostil on gastric acid and pepsin secretion in man: a review of studies in healthy volunteers.

The antisecretory effect of rioprostil on acid and pepsin secretion stimulated by pentagastrin or a meal, or on the 24-h intragastric acidity is tested in four different studies in 33 healthy male volunteers using a double-blind, crossover design. The oral doses of rioprostil used are 50 micrograms, 100 micrograms, 150 micrograms, 200 micrograms, 300 micrograms and 600 micrograms; these are the results obtained: Rioprostil reduces basal H+ and pepsin output by more than 50%. Rioprostil, 300 micrograms and 600 micrograms, significantly reduces the 3-h pentagastrin-stimulated acid output by 43.5% and 58.9%, respectively, and the 3-h stimulated pepsin output by 41.1% and 66.5%, respectively (p = 0.01). Depending on the method used for intragastric titration the following percentages of inhibition of acid secretion are observed, 40%, 65%, and 75% with 150 micrograms, 300 micrograms, and 600 micrograms rioprostil respectively, with one method and 32%, 34%, and 79% with 25 micrograms, 50 micrograms, and 200 micrograms rioprostil respectively, with a somewhat modified technique. The differences observed in % inhibition between these two studies can be explained by the use of a different intragastric titration technique. Rioprostil, 300 micrograms and 600 micrograms, significantly inhibits night-time acid secretion (AUC x h, 2400 h-0800 h) by 52% and 73.5% when compared with placebo (p = 0.03). The calculated ED50 for acid inhibition is 86.5 micrograms of rioprostil.

Adult↗
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↗