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Biomedical subjects

J Oleksy

Publications and source records attributed to J Oleksy.

At least 19 recordsLinked to original sources
PubMed1994

[Comparative evaluation of culture techniques and ELISA test in detection of Helicobacter pylori infection].

The paper evaluates the correlation between culture tested for Helicobacter pylori from biopsy material obtained from patients diagnosed with stomach ulcer, duodenal ulcer and gastritis, and the level of specific IgG antibodies measured by the ELISA test. As compared with culture, the ELISA test yielded a higher percentage of positive assays. Antibody titer was particularly raised in patients with duodenal ulcer, which accounted for 83% of cases. The highest frequency of positive cultures (50%) was also obtained in this group of patients. Essentially, the results are in agreement with findings reported by other authors.

Adult↗
PubMed1993

Effects of ebrotidine on aspirin-induced gastric mucosal damage and blood flow in humans.

Nonsteroidal anti-inflammatory agents (NSAIDs) such as aspirin (ASA) damage the gastric mucosa both in normal subjects and in arthritic patients. The aim of this study was to investigate the protective action of a new H2-receptor antagonist, ebrotidine, in the prevention of ASA-induced acute mucosal injury in the stomach of healthy volunteers. In a double-blind randomized crossover study 10 male volunteers received treatment with either placebo plus ASA (500 mg) or ebrotidine (800 mg) plus ASA twice daily for 3 days with 10 days' washout period between treatments. The mean number of gastric erosions seen at endoscopy after treatment with ebrotidine plus ASA (2.0 +/- 0.3) was significantly lower than that after placebo plus ASA (3.7 +/- 0.2). This reduction in lesion core by ebrotidine was accompanied by a significant increase in gastric blood flow (by 15% in corpus and 26% in antrum), by a rise in transmucosal potential difference (by 12%), and by a decrease of mucosal microbleeding. Ebrotidine afforded substantial protection from ASA-induced injury to the gastric mucosa, and this was accompanied by increase of the mucosal blood flow. We conclude that ebrotidine provides mucosal protection for patients taking NSAIDs.

Adult↗
PubMed1992

Gastroprotective and antisecretory effects of ebrotidine.

This study was designed to assess the gastroprotective and secretory effects of ebrotidine, a novel H2-receptor antagonist, in humans. Two groups (A and B) of male subjects with normal gastric mucosa were used. Group A (six subjects) was treated for 3 days with either ebrotidine or placebo in a randomized, crossover study, and on the 4th day 100 ml of 50% ethanol was sprayed on the mucosa via an endoscope. Pretreatment with ebrotidine significantly reduced the endoscopic score of mucosal damage and deep hemorrhagic lesions caused by ethanol as compared with those in placebo-treated subjects. In group B (six subjects) the 24-h pH-metry was assessed with an intraluminal pH electrode placed in the gastric corpus and connected to portable recording apparatus. A single oral dose of ebrotidine (800 mg) caused a significant reduction in circadian acidity and resulted in a marked and significant inhibition of acid secretion for about 6 h on administration. We conclude that ebrotidine is highly effective as a gastroprotective agent, and as an H2-receptor antagonist shows a potent inhibitory effect on gastric acid secretion in humans.

Adult↗
PubMed1992

Gastric acid inhibitory profile of ebrotidine, a novel H2-receptor antagonist in humans.

This study was designed to assess the gastric secretory effects of ebrotidine, a novel H2 receptor antagonist, in humans. Three groups (A, B and C) of male subjects with normal gastric mucosa were used. Group A (6 subjects) was used to determine the dose-dependency of gastric inhibitory effect of ebrotidine on basal and pentagastrin-induced maximal acid output. Group B (8 subjects) was employed to examine the duration of the inhibitory effect of ebrotidine on basal and pentagastrin-induced acid secretion. In group C (6 subjects), the 24h pH-metry was assessed using intraluminal pH-electrode placed in the gastric corpus and connected to a portable recording unit. Single oral dose of ebrotidine (200, 400 or 800 mg) caused a dose-dependent reduction in basal and pentagastrin-induced acid secretion that at a dose of 800 mg amounted to about 89% and 93%, respectively. This inhibition was still observed after 6h and averaged 72% and 50%, respectively. After 12 and 24h upon the drug intake, both basal and pentagastrin-induced acid secretion returned to the control values. Single oral dose of ebrotidine (800 mg) caused a significant reduction in circadian acidity and resulted in a marked and significant reduction of intragastric acidity for about 6h upon the administration. This inhibition was accompanied by a transient increase in basal and postprandial gastrin levels. We conclude that ebrotidine is highly effective inhibitor of basal, pentagastrin-induced and circadian gastric acid secretion in humans.

Administration, Oral↗
PubMed1991

Effects of nocloprost on gastric functions in man.

Previous studies in animals and humans demonstrated that nocloprost, a stable prostaglandin E2 analogue, shows very high gastroprotective potency, relatively weak gastric inhibitory activity, and low systemic bioavailability after oral administration. In this study the effects of nocloprost on gastric acid secretion and intraluminal pH and on gastric emptying and plasma gastrin levels were determined in humans. Nocloprost at doses of 50 and 100 micrograms was ineffective, but at a dose of 200 micrograms it reduced the response to pentagastrin significantly and that to a peptone meal by 30-50% and abolished plasma gastrin response without affecting the rate of gastric emptying. Nocloprost given at a dose of 100 micrograms three times daily 30 min before the major meals (breakfast, lunch, and dinner) did not affect intragastric pH significantly as monitored by continuous intraluminal pH-metry. We conclude that nocloprost does not affect gastric acid secretion or intraluminal pH when applied at a dose (50-100 micrograms) that is gastroprotective and that is proposed for peptic ulcer therapy. A higher dose (200 micrograms) of nocloprost causes moderate gastric acid inhibition and suppression of plasma gastrin release without affecting gastric emptying or causing any side effects.

Adult↗
PubMed1991

Gastric protection by nocloprost against aspirin damage in humans. Possible role of epidermal growth factor.

Ten healthy young male subjects took part in a double-blind, placebo-controlled crossover study to assess the effects of nocloprost on gastric microbleeding and endoscopic mucosal injury induced by the administration of aspirin (2.5 g). In addition, basal and pentagastrin-induced gastric acid and pepsin secretion and salivary and plasma contents of epidermal growth factor (EGF) were measured after placebo plus aspirin or nocloprost plus aspirin treatment in these subjects. Nocloprost (100 micrograms/dose) significantly reduced spontaneous gastric microbleeding and almost completely prevented gastric mucosal injury induced by aspirin. Nocloprost failed to affect basal and pentagastrin-stimulated gastric acid and pepsin secretion but increased significantly the salivary outputs and plasma concentrations of EGF. In conclusion, nocloprost is effective in preventing gastric injury by aspirin even at a non-antisecretory dose, and this protection may involve an excessive release of EGF.

Adult↗
PubMed1990

Cholecystokinin in the inhibition of gastric secretion and gastric emptying in humans.

Cholecystokinin (CCK) is known to inhibit gastric acid secretion and gastric emptying but its physiological role in the inhibition of gastric functions is not settled. In this study performed on 16 young male subjects, gastric acid secretion and emptying rate were determined after intragastric administration of 8% peptone meal alone or in combination with intravenous infusion of graded doses of CCK-8 (5-80 pmol/kg.h) or with addition of vegetable oil to meal without or with pretreatment with loxiglumide, a specific CCK antagonist. CCK-8 infusion at lower dose (5 pmol/kg.h) was ineffective but at higher doses (20-80 pmol/kg.h) it resulted in a significant reduction in acid output by 39 and 43% and a decrease in gastric emptying from 54% to 40 and 22%, respectively. Pretreatment with loxiglumide abolished almost completely the inhibition of both gastric acid and gastric emptying by CCK-8. Fat added to peptone meal reduced gastric acid secretion by 42-65% and decreased gastric emptying to 24-32%. The pretreatment with loxiglumide tended to reduce fat-induced inhibition of gastric acid secretion and gastric emptying but the difference in the inhibition of gastric functions between the tests without and with loxiglumide was not significant. This study provides evidence that exogenous CCK administered at pharmacological doses is a potent inhibitor of gastric acid secretion and gastric emptying and probably acts via specific CCK receptors. In contrast, fat induces inhibition of gastric acid secretion and gastric emptying that cannot be fully attributed to hormonally acting CCK.

Adult↗
PubMed1989

CCK receptor antagonism by loxiglumide and gall bladder contractions in response to cholecystokinin, sham feeding and ordinary feeding in man.

The postprandial contractions of the gall bladder result from the interaction of neurohormonal factors but their relative contribution is unknown. This study was designed to determine the role of cholecystokinin (CCK) in gall bladder contractions using a highly selective and potent CCK-receptor antagonist, CR-1505 (loxiglumide) in healthy men either infused with exogenous CCK in graded doses (1.56-50 pmol/kg/h) or subjected to modified sham feeding (MSF) and ordinary feeding tests. The gall bladder volume measured by real time ultrasonography showed dose dependent decrease in the gall bladder volume in 10 subjects when CCK8 was infused iv in graded doses reaching about 15% at 1.56 pmol/kg/h and 91% at 50 pmol/kg/h. Close correlation between the decrease in gall bladder volume and the dosage of CCK or the increments in plasma CCK-bioactivity was observed. After pretreatment with loxiglumide, CCK resulted in similar increments in plasma CCK-bioactivity but failed to affect the gall bladder volume at CCK doses up to 6.25 pmol/kg/h and caused only 53% reduction at 50 pmol/kg/h. Modified sham feeding and real feeding reduced the volume of gall bladder by 20% and 70%, respectively and loxiglumide decreased these values to 15% and 30%, respectively. This study provides evidence that loxiglumide is highly potent and selective CCK antagonist and that endogenous CCK plays an important role both in the postprandial contractions of gall bladder.

Adolescent↗
PubMed1989

Distribution and release of epidermal growth factor in man.

Epidermal growth factor (EGF) is localised in man to salivary and Brunner's glands. It is present in large concentrations in saliva and duodenal contents but the mechanisms of its release have been little studied. This study carried out on four groups of healthy subjects was designed to determine the distribution and the release of immunoreactive EGF (IR-EGF) in salivary, gastric, duodenal, and pancreatic secretions. Under basal conditions, the concentrations of IR-EGF in salivary, gastric, duodenal and pancreatic secretions were; 2.7 (0.4), 0.42 (0.12), 21 (5) and 8.5 (1.2) ng/ml, respectively. Chewing of Parafilm* significantly increased salivary but not gastric or duodenal EGF output while atropinisation led to the reduction in basal salivary and duodenal EGF output without affecting the increment in EGF release induced by chewing. Cigarette smoking caused a marked reduction in basal salivary and duodenal EGF output. Infusion of pentagastrin increased salivary and duodenal EGF output and this was blocked by the addition of somatostatin. Injection of secretin lead to an increase in pancreatic output of EGF. We conclude that in man the major sources of EGF are salivary glands, duodenum, and pancreas and that the release of EGF remains under neurohormonal control.

Adult↗
PubMed1989

Release and action of epidermal growth factor on gastric secretion in humans.

Epidermal growth factor (EGF) has recently been localized in salivary, pancreatic, and Brunner's glands in humans, but little is known about its release and its action on gastric secretion. This study, performed on healthy subjects, was designed to determine the release of immunoreactive EGF in plasma and in salivary and gastric secretions under basal conditions and after modified sham feeding (MSF), ordinary feeding, and infusion of pentagastrin without and with addition of exogenous recombinant human EGF (hEGF). Under basal conditions the EGF concentrations in plasma and salivary and gastric secretions were 52 +/- 8 pg/ml, 2.5 +/- 0.3 ng/ml, and 0.12 +/- 0.03 ng/ml, respectively. MSF and ordinary feeding increased significantly EGF plasma level and salivary output but not gastric EGF output, and atropinization failed to effect these plasma and salivary EGF responses to MSF. Intravenous infusion of pentagastrin increased both plasma and salivary but not gastric EGF, and addition of exogenous hEGF in graded doses (0.25-1.0 micrograms/kg) resulted in a dose-dependent increase in the plasma level of EGF and in significant inhibition of gastric acid and pepsin outputs. The increment in plasma EGF, which resulted in significant inhibition of gastric secretion, was several times greater than that observed after MSF or feeding. EGF infused in a constant dose (0.12 or 1.0 micrograms/kg-h) resulted in an increment in plasma EGF similar to that observed after MSF alone.

Adult↗
PubMed1988

Effects of colloidal bismuth subcitrate on aspirin-induced gastric microbleeding, DNA loss, and prostaglandin formation in humans.

Ten healthy young male subjects took part in a double-blind, placebo-controlled, crossover trial to assess the effect of colloidal bismuth subcitrate (De-No) on prostaglandin (PG) E2 generation and mucosal integrity in an aspirin (ASA)-treated stomach. After administration of ASA (2.5 g) plus placebo, a marked reduction in mucosal generation of PGE2 (by about 85%) was observed, and this was accompanied by a significant increase in gastric microbleeding and DNA loss and endoscopic and histologic damage of the mucosa. After the combination of De-Nol (300 mg four times daily) with ASA, mucosal generation of PGE2 showed a reduction similar to that in tests with ASA plus placebo, but gastric microbleeding and mucosal damage were significantly reduced. It is concluded that De-Nol has a protective action on ASA-induced gastric microbleeding and that this protection occurs despite a marked suppression of mucosal production of prostaglandins.

Anti-Ulcer Agents↗
PubMed1987

De-Nol stimulates gastric and duodenal alkaline secretion through prostaglandin dependent mechanism.

This study was designed to determine the effects of colloidal bismuth subcitrate De-Nol on gastric HCO3- secretion in 24 healthy subjects and on gastric and duodenal HCO3- secretion in dogs with gastric and duodenal fistulae. Alkaline secretion was measured after pretreatment with ranitidine to abolish the H+ secretion using a constant perfusion aspiration system and back titration of the perfusates to the original pH 6.0. Luminal release of PGE2 was also measured in the gastric and duodenal perfusates. Addition of De-Nol in gradually increasing concentrations resulted in step wise increments in gastric HCO3- secretion in man and in dogs reaching, respectively, about 80% and 55% of the maximal HCO3- response to 16, 16dimethyl-PGE2 (dmPGE2). The duodenal HCO3- response to De-Nol in dogs reached 72% of the dmPGE2 maximum. These effects were accompanied by a significant increase in luminal release of PGE2. Pretreatment with atropine reduced basal and in part De-Nol induced alkaline secretion, whereas pirenzepine did not affect this secretion in man and dogs. Aspirin (in man) and indomethacin (in dogs) reduced the release of PGE2 by about 80% and suppressed almost completely the gastric and duodenal HCO3- response to De-Nol in these species. This study provides evidence that De-Nol stimulates gastroduodenal alkaline secretion through a prostaglandin dependent mechanism.

Adult↗
PubMed1987

Vagal cholinergic control of gastric alkaline secretion in normal subjects and duodenal ulcer patients.

Gastric alkaline secretion was determined in ranitidine treated healthy subjects and duodenal ulcer (DU) patients using gastric perfusion aspiration system and back titration of gastric perfusate to original pH 6.0. Basal alkaline secretion showed periodic fluctuations reaching peaks at phase III of the migrating motor complex (MMC) in the stomach. Mean basal alkaline secretion in healthy normals and DU patients averaged 1120 +/- 124 and 880 +/- 72 mumol/h, respectively and no correlation was found between basal and maximally stimulated gastric acid and alkaline secretion. Modified sham feeding in normal subjects and in DU patients increased this secretion to the peaks of about 28 and 36% of the maximal alkaline response to intragastric application of 16,16 dimethyl-PGE2 in these subjects. Vagotomy did not affect significantly basal alkaline secretion but prevented the rise in alkaline secretion induced by modified sham feeding. Atropine (5-20 micrograms/kg) decreased dose dependently basal, and prevented the modified sham feeding induced alkaline secretion, while pirenzepine (5-20 micrograms/kg) had little influence on basal, and did not affect the modified sham feeding induced, alkaline secretion. This study shows that basal gastric alkaline secretion fluctuates in phase with gastric motor activity, and is similar in normal and DU patients. Vagal stimulation strongly increases alkaline secretion, the effect being abolished by vagotomy and atropine, but not by pirenzepine, suggesting the involvement of M2 rather than M1 subtypes of muscarinic receptors in this stimulation.

Adult↗
PubMed1987

Effects of protective drugs on gastric alkaline secretion in man.

This study was designed to determine the effects of sucralfate, De-Nol, and Maalox 70 on gastric HCO3 secretion in 34 healthy humans. Alkaline secretion was measured after pretreatment with ranitidine to abolish H+ secretion, using a constant perfusion-aspiration system and back-titration of the perfusates to the original pH 6.0. Luminal release of PGE2 was also measured in the gastric perfusates. Addition of sucralfate or De-Nol resulted in increments of gastric HCO3 secretion, reaching about 45% and 59%, respectively, of the maximal HCO3 response to 16,16-dimethyl PGE2 (dmPGE2). The highest response to Maalox 70 reached about 21% of dmPGE2 maximum. These effects of sucralfate, De-Nol, and Maalox 70 were accompanied by a significant increase in luminal release of PGE2. Pretreatment with atropine reduced basal and, in part, sucralfate-, De-Nol-, and Maalox 70-induced alkaline secretion, whereas pirenzepine did not affect this secretion. Aspirin reduced the release of PGE2 by about 80% and suppressed almost completely the gastric HCO3 response to sucralfate, De-Nol, and Maalox 70. This study provides evidence that sucralfate, De-Nol, and Maalox 70 stimulate gastric alkaline secretion via a prostaglandin-dependent mechanism.

16,16-Dimethylprostaglandin E2↗
PubMed1987

Gastroprotection by sucralfate against acetylsalicylic acid in humans. Role of endogenous prostaglandins.

Sucralfate has been shown to prevent the formation of acute gastric lesions induced by nonsteroidal antiinflammatory drugs such as aspirin (ASA) in animals, but little is known about the prevention by this agent of ASA-induced gastric damage in humans. This report describes the effects of sucralfate on mucosal formation of prostaglandins (PG), gastric microbleeding and DNA loss in intact and ASA-challenged stomach. Two groups of 12 healthy volunteers were used in a double-blind, placebo controlled trial to assess the effects of sucralfate 1.0g qid on the stomach in subjects without (group A) and with administration of 2.5g ASA during 2 days (group B). Sucralfate treatment during 4 days significantly reduced spontaneous gastric bleeding and DNA loss in group A and prevented blood loss caused by ASA in group B. The protective effects of sucralfate on spontaneous gastric blood loss were accompanied by increased mucosal biosynthesis and luminal release of PGE2 and 6-keto-PGF1 alpha with decreased release of TXB2. In ASA-treated subjects mucosal generation and luminal release of PG and TXB2 were greatly suppressed and sucralfate treatment did not influence these PGs in spite of the decreased mucosal damage. It is concluded that sucralfate has a potent protective action on spontaneous and ASA-treated gastric bleeding in man and that this protection may be partly due to the increased mucosal biosynthesis of prostaglandins.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Double blind controlled study on the effect of sucralfate on gastric prostaglandin formation and microbleeding in normal and aspirin treated man.

Two groups A and B each comprising 12 healthy young male subjects were used in a double blind, placebo controlled trial to assess the effects of 1.0 g sucralfate qid on prostaglandin (PG) generation and mucosal integrity in the intact and aspirin-treated stomach. Mucosal formation and luminal release of PGE2, 6-keto-PGE1 alpha and thromboxane B2, gastric microbleeding and DNA loss (integrity indicators) and basal and pentagastrin induced acid secretion were measured after placebo and sucralfate treatment in subjects without (group A) and with administration of 2.5 g aspirin (group B). Sucralfate significantly reduced spontaneous gastric microbleeding and DNA loss in group A and prevented blood loss but not DNA loss caused by aspirin in group B. The protective effects of sucralfate on spontaneous gastric microbleeding were accompanied by increased mucosal biosynthesis and luminal release of PGE2 and 6-keto-PGF1 alpha with a reduction in release of thromboxane B2. In aspirin treated subjects both mucosal generation and luminal release of prostaglandins and thromboxane B2 were greatly suppressed although sucralfate treatment did not influence these prostaglandins in spite of the reduction in mucosal damage. It is concluded that sucralfate has a potent protective action on spontaneous and aspirin treated gastric microbleeding in man and that this protection may be partly because of the increased mucosal biosynthesis of prostaglandins.

Adult↗
PubMed1985

Effects of somatostatin-14 and somatostatin-28 on plasma hormonal and gastric secretory responses to cephalic and gastrointestinal stimulation in man.

This study was designed to determine the influence of cephalic and gastrointestinal meal stimulation on plasma levels of somatostatin-like immunoreactivity (SLI) and to compare plasma hormonal and gastric secretory effects of somatostatin-14 (SS-14) and its putative prohormone, somatostatin-28 (SS-28), in humans. Cephalic stimulation induced by modified sham feeding did not affect plasma SLI, whereas a gastric liver extract meal caused a significant increase in SLI. Infusion of SS-28 dose-dependently suppressed gastric acid, serum gastrin, and plasma pancreatic polypeptide (PP) responses to cephalic and gastrointestinal stimulation. SS-28 was equipotent with SS-14 as gastric inhibitor when compared on the basis of molar doses infused but was 4-10 times less potent on the basis of plasma SLI concentrations obtained. A lower and more physiological dose of SS-14 (75 pmol/kg-h) reduced gastric acid and PP responses but failed to affect the serum gastrin response to a meal; whereas a larger, pharmacological dose (500 pmol/kg-h) also suppressed serum gastrin responses. We conclude that meal releases SLI into the circulation and that SS-28 mimics the gastric secretory and plasma hormonal effects of SS-14 but is several times less potent than SS-14 in terms of circulating hormone levels.

Adult↗