[Case of carcinoid tumor of the bronchus].
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Bronchi↗
Biomedical subjects
J Oleksy
Publications and source records attributed to J Oleksy.
Action of omeprazole (a benzimidazole derivative) on secretory responses to sham feeding and pentagastrin and upon serum gastrin and pancreatic polypeptide in duodenal ulcer patients.
The effects of omeprazole, a benzimidazole derivative, have been determined on the secretory responses to modified sham feeding and pentagastrin, and upon serum gastrin and pancreatic polypeptide concentrations in duodenal ulcer patients. Intragastric administration of omeprazole in doses of 2 and 6 mumol/kg produced, respectively, about 50% and 90% reduction in acid outputs in responses to modified sham feeding and pentagastrin without affecting serum gastrin and pancreatic polypeptide response to modified sham feeding.
Adult↗
Effect of meciadanol on gastric secretion and aspirin-induced gastric mucosal injury in humans.
The aim of this study was to assess the effects of a newly synthesized flavonoid, meciadanol, on gastric secretion and on aspirin-induced gastric mucosal injury in healthy humans. In vitro experiments have shown that meciadanol (INN proposed) inhibits histidine decarboxylase in gastric cells. In our study meciadanol did not affect either basal or pentagastrin-stimulated gastric acid secretion or pepsin secretion and did not produce any endoscopic or histological changes in the stomach or duodenum. Meciadanol prevented aspirin-induced microbleeding and aspirin-induced DNA loss, suggesting that gastric mucosal histamine is involved in the mucosal injury caused by aspirin.
Adult↗
Prostaglandins in peptic ulcer disease: effect of nonsteroidal anti-inflammatory compounds (NOSAC).
This study shows that human fundic mucosa generates various PGs, particularly PGE2, and thromboxanes and this generation appears to be significantly lower in gastric ulcer than in duodenal ulcer patients or normal subjects. Non-steroidal antiinflammatory compounds (NOSAC), such as aspirin and indomethacin, greatly reduce the PG biosynthesis and cause mucosal damage including mucosal erosions and haemorrhages observed at endoscopy, increased gastric microbleeding and DNA loss. In contrast, carprofen, a novel NOSAC with good antiinflammatory properties and gastric tolerance, failed to affect mucosal generation of PGs and did not influence gastric mucosal integrity. This study indicates that the deficiency of endogenous PGs may play a role in the pathogenesis ulcer and that the degree of gastric mucosal damage by NOSAC is closely related to the alteration in the capability of the mucosa to generate PGs.
Adult↗
Generation of prostaglandins in gastric mucosa of patients with peptic ulcer disease: effect of nonsteroidal antiinflammatory compounds.
Human fundic mucosa generates various prostaglandins (PGs), particularly PGE2, and tromboxanes. This generation appears to be significantly lower in gastric ulcer patients than in duodenal ulcer patients or normal subjects. Nonsteroidal antiinflammatory compounds (NOSAC), such as aspirin or indomethacin, greatly reduce the PG biosynthesis and cause mucosal damage, including mucosal erosions and hemorrhages observed at endoscopy, increased gastric microbleeding and DNA loss. In contrast, paracetamol or carprofen, a novel NOSAC, fails to affect mucosal generation of PGs and does not influence gastric mucosal integrity. This study indicates that endogenous PGs may be involved in the pathogenesis of gastric ulcer and that normal generation of mucosal PGs is essential for the mucosal integrity.
Adult↗
Comparison of prostaglandin E2 and ranitidine in prevention of gastric bleeding by aspirin in man.
This study was designed to compare the effect of oral administration of PGE2 (0.5 mg/kg) and ranitidine in larger (100 mg/dose) or smaller (10 mg/dose) doses on aspirin-induced gastric microbleeding and DNA loss determined chemically in gastric washings in eight healthy subjects. Aspirin (0.5 g) given four times daily greatly increased the rate of gastric bleeding and DNA loss and pretreatment with PGE2 or ranitidine in larger doses almost completely prevented these changes. Smaller non-antisecretory doses of ranitidine also reduced the rate of bleeding and DNA loss but to a lesser degree than PGE2. This study confirms that oral PGE2 has a protective action on gastric mucosa exposed to aspirin and that this property is also shared by ranitidine, a potent histamine H2-receptor antagonist.
Adult↗
Effect of enkephalin and naloxone on gastric acid and serum gastrin and pancreatic polypeptide concentrations in humans.
The effects of a synthetic enkephalin analogue with prolonged opioid activity, D-ala-2-enkephalin (ala-enk) and naloxone given alone or in combination, on vagally, pentagastrin- and histamine-induced gastric secretion and plasma hormonal responses to vagal stimulation have been studied in healthy subjects. D-ala-2-enkephalin reduced basal gastric acid and pepsin secretion, and caused a dose-dependent inhibition of gastric secretory responses to modified sham-feeding and pentagastrin but not to histamine. It increased serum gastrin concentration and suppressed plasma pancreatic polypeptide response to modified sham-feeding. Naloxone alone at lower dose levels did not affect gastric secretion and plasma hormonal concentrations but at higher doses it reduced both basal and modified sham-feeding-induced secretion. When combined with ala-enk it reversed in part gastric secretory and plasma hormonal changes induced by this peptide during modified sham-feeding and pentagastrin stimulation. These results indicate that (1) stable enkaphalin analogue inhibits basal and vagally or pentagastrin-induced gastric secretion, and affects plasma hormonal response to vagal stimulation, at least in part, via activation of opioid receptors and (2) endogenous opioid substances may be involved in the stimulation of gastric secretion in man.
Adult↗
Prostaglandins and vagal stimulation of gastric secretion in duodenal ulcer patients.
The effects of a stable prostaglandin (PG) E2 analog (15-R-15 methyl PGE2) and aspirin, a potent inhibitor of cyclooxygenase, on modified sham-feeding (MSF)-stimulated gastric secretion and serum gastrin and pancreatic polypeptide (PP) levels were measured in patients with duodenal ulcer. PGE2 analog given orally significantly reduced gastric acid and pepsin secretion and suppressed serum PP but not gastrin responses to MSF. Suppression of PG generation in the gastric mucosa did not influence the secretory or hormonal responses to MSF. This study shows that endogenous PGs are not involved in the control of vagally stimulated gastric secretion, but exogenous PGE2 analog is an effective inhibitor of such secretion and merits clinical evaluation in the treatment of duodenal ulcer.
Adult↗
Effect of enkephalin and naloxone on vagal and hormonal stimulation of pancreatic secretion in man.
Pancreatic secretory responses to modified sham-feeding (MSF) and secretin (1 U/kg-h) infusion were examined in eight healthy subjects with and without administration of the stable enkephalin analogue (Ala-Enk) and/or naloxone. MSF produced a clear increase in pancreatic protein output, reaching about 45% of caerulein (0.5 microgram/kg-h) maximal output. This response was significantly reduced by Ala-enk (20 micrograms/kg-h) but was not affected by naloxone (40 micrograms/kg-h). Ala-Enk given during a well-sustained plateau of pancreatic response to secretin also significantly suppressed both bicarbonate and protein; the effect was not influenced by the addition of naloxone. Naloxone alone without Ala-Enk did not affect basal or stimulated pancreatic secretion. We conclude that enkephalin inhibits pancreatic secretion induced by vagal or secretin stimulation, and this inhibition does not seem to be mediated by opiate receptors of the mu type, since naloxone was ineffective in the prevention of this effect.
Adult↗
The use of carprofen, a non-steroidal antiinflammatory agent, in peptic ulcer diseases.
The effects of carprofen (Roche), a nonsteroid antiinflammatory agent, on gastric secretion, serum gastrin level, electropotential difference (PD), gastric microbleeding, DNA loss, and the generation of mucosal prostaglandins (PGs) were examined in 20 duodenal ulcer patients with active ulcer (15 patients) or in remission (5 patients). Carprofen administered for one-week period at a therapeutic dose (300 mg/day) was well tolerated by all ulcer patients and no adverse effects were observed during or after treatment. Endoscopy performed after carprofen treatment showed complete ulcer healing in 9 out of 15 patients and no exacerbations were observed in the rest of patients. No significant changes were observed in basal or pentagastrin-induced secretion, PD, gastric microbleeding and DNA loss. The generation of PGE2, 6-keto-PGF1 alpha and thromboxane B2 was not affected by the treatment with carprofen. This study indicates that carprofen shows excellent gastrointestinal tolerance in ulcer patients, and it might be useful in the treatment of arthritic patients with peptic ulcer disease.
Action Potentials↗
Effect of human pancreatic polypeptide and its C-terminal hexapeptide on pancreatic secretion in man and in the dog.
Human pancreatic polypeptide (HPP) and its C-terminal hexapeptide (HP-PP) were infused intravenously in graded doses into healthy human subjects and dogs with chronic pancreatic fistula during submaximal stimulation with secretin. Plasma levels of PP were measured by radioimmunoassay, and pancreatic volume flow and bicarbonate and protein outputs were monitored. PP and HP-PP in humans did not affect secretion-induced volume flow or bicarbonate secretion, but at the highest doses it reduced the protein outputs. In dogs both HPP and HP-PP inhibited dose-dependently the pancreatic volume flow and bicarbonate and protein outputs. There was a linear correlation between the dose of HPP infused and the increments in plasma PP levels in these experiments. The inhibition of pancreatic secretion occurred at doses of exogenous HPP which produced blood plasma PP concentrations not significantly different from those normally seen after a meat meal. We conclude that there is a marked difference in the effect of HPP on the exocrine pancreas in man and the dog, that PP may play a role as a physiological inhibitor of pancreatic protein secretion in man and of both bicarbonate and protein secretion in the dog, and that the effect of HPP on the exocrine pancreas can be mimicked by its C-terminal hexapeptide.
Adult↗
Effect of carprofen and indomethacin on gastric function, mucosal integrity and generation of prostaglandins in men.
The effects of indomethacin and carprofen on gastric secretion, serum gastrin level, electropotential difference, gastric microbleeding, DNA loss, mucosal blood flow and the production of mucosal prostaglandins (PGs) were investigated in a double-blind cross-over study in 18 healthy volunteers after one week of treatment. We did not observe any significant changes in basal and pentagastrin-stimulated gastric secretory parameters, serum gastrin level and electro-potential difference before and after treatment with these drugs. Mucosal blood flow was significantly reduced following indomethacin treatment. The most pronounced differences were found in endoscopic score studies of gastric mucosa. After indomethacin all subjects developed multiple erosions, submucosal haemorrhages, and half of them showed diffuse antral erythema. These effects were accompanied by a significant increase in both gastric microbleeding and DNA loss, and significant decrease in the production of PGE2. We concluded that carprofen, in contrast to indomethacin, did not alter gastric mucosal integrity and production of PGE2. This study indicates that the gastric mucosal damage by non-steroid anti-inflammatory compounds (NOSAC) depends upon the suppression of PGE2 biosynthesis, and that endogenous PGE2 is involved in the control of mucosal blood flow and mucosal integrity.
Adult↗
Gastric secretory and plasma hormonal responses to sham-feeding of varying duration in patients with duodenal ulcer.
Gastric acid and serum gastrin, pancreatic polypeptide, and insulin responses to cephalic vagal stimulation were studied in eight patients with duodenal ulcer using modified sham-feeding for periods varying from four to 30 minutes. In addition, the maximal acid response to sham-feeding was compared with that induced by pentagastrin in 10 healthy subjects and 14 patients with duodenal ulcer. It was found that the gastric acid response to modified sham-feeding reached the maximal value after 15 minutes of sham-feeding and amounted to about 68% of the pentagastrin maximum. The serum pancreatic polypeptide response was also increased after modified sham-feeding and depended on the duration of this procedure, whereas gastrin and insulin responses were not significantly affected by modified sham-feeding. When the peak acid output induced by modified sham-feeding was normalised as percentage of the peak response to pentagastrin, it was similar in healthy subjects and in patients with duodenal ulcer; this indicates that the increased peak acid response to modified sham-feeding observed in patients with duodenal ulcer corresponded with their greater parietal cell mass rather than with increased vagal tone.
Adult↗
Distribution of prostaglandins in gastric and duodenal mucosa of healthy subjects and duodenal ulcer patients: effects of aspirin and paracetamol.
The distribution of mucosal PGE2-like activity was determined by bioassay technique in the body and antrum of the stomach and in the duodenum of healthy subjects and duodenal ulcer patients before and after administration of aspirin, paracetamol, or histamine. In healthy subjects, the oxyntic, antral and duodenal mucosa was found to be capable of generating large amounts of PGE2, which were not significantly different from those found in duodenal ulcer patients. No correlation was found between the generation of PGE2 and gastric acid secretory status or serum gastrin level. Aspirin-and to a much lesser extent, paracetamol-caused a dramatic reduction in the ability of the gastric mucosa to biosynthesis PGE2 and this was accompanied by marked side-effects and injury to the gastric mucosa. Administration of histamine caused small but significant reduction in the biosynthesis of PGE2 but it was accompanied by marked mucosal damage. This study indicates that the gastric and duodenal mucosa is capable of generating PGE2-like activity which may be involved in the mechanism that protects the mucosa against the damage caused by aspirin.
Acetaminophen↗
Dynamics of gastric acid inhibition by ranitidine in duodenal ulcer patients.
The dynamics of the inhibitory effect of ranitidine, a new H2-receptor antagonist, on histamine and pentagastrin-induced gastric secretion have been examined in duodenal ulcer patients. The inhibition by ranitidine of histamine-induced secretion was found to be competitive, whereas that of pentagastrin-induced secretion not competitive. Ranitidine was an effective inhibitor of pentagastrin-induced secretion for 8-12 h after administration. The availability of ranitidine, a powerful and long-acting inhibitor of gastric secretion, provides an opportunity of an alternative treatment from cimetidine for peptic ulcer and related diseases.
Adult↗
Kinetics and duration of action of ranitidine on gastric secretion and its effect on pancreatic secretion in duodenal ulcer patients.
Inhibitory effects of ranitidine, a new H2-receptor antagonist, and cimetidine on histamine and pentagastrin-induced gastric secretion have been compared in duodenal ulcer patients. Compared with cimetidine, ranitidine was found to be about 6-8 times a more potent inhibitor of gastric acid secretion, the inhibition of histamine-induced secretion being competitive, whereas that of pentagastrin-induced secretion not competitive. Ranitidine was an effective inhibitor of pentagastrin-induced secretion 8-12 h after administration. When given in a dose inhibiting gastric secretion by over 90%, it did not affect pancreatic secretion induced by secretin and pancreozymin. The availability of ranitidine, a more powerful inhibitor of gastric secretion, provides an opportunity of a treatment alternative to cimetidine, for peptic ulcer and related diseases.
Adult↗
Effect of ranitidine, a new H2-antagonist, on gastric and pancreatic secretion in duodenal ulcer patients.
The effects of a new H2-receptor blocker, ranitidine, given intravenously (for comparison with cimetidine) or orally an gastric and pancreatic secretion have been studied in duodenal ulcer patients. Ranitidine appears to be several times more potent and a longer-acting inhibitor of gastric secretion than cimetidine. This H2 blocker does not affect pancreatic bicarbonate and enzyme secretion.
Administration, Oral↗
Comparison of ranitidine and cimetidine in the inhibition of histamine, sham-feeding, and meal-induced gastric secretion in duodenal ulcer patients.
The effects of ranitidine, a new H2-receptor antagonist which does not contain an imidazole ring, and cimetidine have been determined on histamine, meal-induced gastric acid secretion, and serum gastrin levels in duodenal ulcer patients. Compared with cimetidine, ranitidine was found to be about eight times more potent an inhibitor of histamine-induced secretion and four to five times more potent an inhibitor of sham-feeding, and real feeding induced acid secretion without effecting serum gastrin levels.
Adult↗