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Biomedical subjects

A Aly

Publications and source records attributed to A Aly.

At least 55 records · Page 3Linked to original sources

Prostaglandin synthesis in the human gastrointestinal mucosa.

Prostaglandins derive from polyunsaturated fatty acids, of which arachidonic acid is the most abundant. Arachidonic acid occurs in all cell membranes, where it is bound to phospholipids and can, once liberated by phospholipases, be metabolized by cyclooxygenase into prostaglandins and thromboxanes and by lipoxygenases into hydroxyacids, leukotrienes and lipoxins. In most studies on prostaglandin formation in the human gastrointestinal mucosa PGE2 and PGF2 alpha seem to be the regularly occurring products. Quantification of mucosal prostaglandin synthesis in vivo is problematic. Mechanical handling of tissues immediately activates arachidonic acid metabolism, and the determination of "tissue levels" of prostaglandins or prostaglandin biosynthesis in biopsy specimens ex vivo thus becomes unreliable as a measure of in vivo formation. A more reliable approach may be to measure prostaglandins in gastrointestinal luminal contents, which can be obtained atraumatically. Most measurements are made by radioimmunological methods, but the specificity of most assays has not been satisfactorily examined. More specific methods such as gas chromatography-mass spectrometry should be used to validate of a radioimmunoassays. Prostaglandin E2, which can be measured by gas chromatography-mass spectrometry, is regularly found in human gastroduodenal luminal contents. Exposure of the mucosa to hydrochloric acid increases the output of PGE2 to the lumen, indicating increased mucosal PGE2 formation during physiological activation of mucosal defense mechanisms.

Arachidonic Acid↗

Indomethacin inhibits duodenal mucosal bicarbonate secretion and endogenous prostaglandin E2 output in human subjects.

Nonsteroidal anti-inflammatory drugs are a frequent cause of gastric and duodenal mucosal injury. We examined the effect of indomethacin on duodenal mucosal bicarbonate secretion and prostaglandin output in healthy subjects. Subjects received either 50 mg of indomethacin or placebo orally 13 hours and 1 hour before study. A 4-cm segment of proximal (the duodenal bulb) or distal (10 to 14 cm beyond the pylorus) duodenum was isolated and perfused with 154 mM NaCl containing a nonabsorbable marker. In the proximal duodenum indomethacin reduced both basal and acid-stimulated bicarbonate secretion by approximately 65% (p less than 0.01); in the distal duodenum indomethacin decreased basal and acid-stimulated bicarbonate output by approximately 45% (p less than 0.01). Oral indomethacin inhibited basal and acid-stimulated duodenal prostaglandin E2 output in both the proximal and distal duodenum. We conclude that, by decreasing duodenal mucosal bicarbonate production and prostaglandin output in humans, oral indomethacin, in two doses of 50 mg each, impairs an important duodenal defense mechanism.

Administration, Oral↗

Acid and pepsin responses to graded doses of pentagastrin in duodenal and corporeal gastric ulcer patients before and after selective proximal vagotomy.

The dose response curves for acid and pepsin output to increasing intravenous doses of pentagastrin (0.01, 0.02, 2, 8, and 16 micrograms/kg per hour) were determined in six male patients with duodenal ulcer and six with type 1 corporeal gastric ulcer before and 3 to 6 months after selective proximal vagotomy and excision of the gastric ulcer. The maximal secretory capacity (maximal response) of acid and pepsin was greater in the duodenal ulcer patients than in the corporeal gastric ulcer patients, but the sensitivity of the oxyntic and peptic cells to pentagastrin (the dose required for half the maximal response) was equal for the two ulcer groups. Selective proximal vagotomy reduced the acid response to insulin by 96 to 100 percent. The acid secretory capacity and the sensitivity of the oxyntic cells to pentagastrin was reduced by selective proximal vagotomy to the same extent in the duodenal ulcer patients and the corporeal gastric ulcer patients. Selective proximal vagotomy reduced the pepsin secretory capacity in the duodenal ulcer patients but did not reduce the already low capacity in the corporeal gastric ulcer patients. Selective proximal vagotomy decreased the sensitivity of the peptic cells in both ulcer groups. Similar results were obtained when the dose response curves were analyzed according to Michaelis-Menten kinetics. Our results justify clinical trials of selective proximal vagotomy with complete ulcer excision for treatment of type 1 corporeal gastric ulcer.

Adult↗

Acid instillation increases gastric luminal prostaglandin E2 output in man.

The capacity of the gastroduodenal mucosa to maintain integrity when exposed to acid and pepsin may require formation of endogenous prostaglandins (PG). The gastric mucosa is capable of PG biosynthesis, and PGE2 is present in the gastric contents of man. The purpose of this study was to examine if acidification of the human stomach affects the output of PGE2. Gastric perfusion was made with 150 mM HCl in seven healthy subjects pretreated with a histamine-2-receptor blocker (ranitidine). Gastric luminal PGE2 was measured by gas chromatography-mass spectrometry. Basal output of PGE2 was 1.42 +/- 0.24 pmol/min (mean + SEM), which increased to 5.37 +/- 0.91 pmol/min (p less than 0.02) during acid perfusion. Gastric acidification did not cause mucosal damage as judged by luminal DNA. We conclude that PGE2 is synthesized in the gastric mucosa even during nearly complete inhibition of parietal cell secretion. Luminal acid, a likely physiological stimulator of mucosal defense, induces a fivefold increase in PGE2 output from the intact mucosa.

Adult↗

Protection of the gastroduodenal mucosa by prostaglandins.

Like other nucleated cell populations in the body, the cells of the gastroduodenal mucosa are capable to metabolise arachidonic acid into prostaglandins, with prostaglandin E2 as the probable major metabolite. The production increases on demand and can be followed in the gastric lumen, where the output of prostaglandin E2 increases two to fourfold after exposure of the mucosa to hydrochloric acid. Exogenous prostaglandins, in particular of the E series, stimulate several identified mucosal defense factors in the upper gastrointestinal tract. Prostaglandins of the E series stimulate the transport of bicarbonate and the production and release of mucus glycoproteins from the gastroduodenal mucosa. They have trophic effects on gastrointestinal epithelia by increasing the survival time of mucosal cells and have cytoprotective properties. In addition, E2 prostaglandins suppress the gastric acid secretion and accelerate peptic ulcer healing. Non steroidal antiinflammatory drugs, which block the biosynthesis of prostaglandins, suppress the bicarbonate secretion, the production of mucus glycoproteins and cytoprotective properties. They interfere with the inhibitory feedback regulation of the gastric acid secretion and are ulcerogenic in experimental and clinical situations. These actions of PG biosynthesis blockers provide indirect information on the importance of local prostaglandin formation for maintenance of gastrointestinal mucosal integrity. It is hypothesised that biosynthesis of prostaglandins in the gastroduodenal mucosa is of importance and may be a key event in triggering the different components of the mucosal defense.

Animals↗

Bioconversion of arachidonic acid in the human gastrointestinal tract.

The data presented demonstrate that the bioconversion of [14C]arachidonic acid in homogenates like these is very easily influenced by protein (enzyme) and substrate concentration as well as exogenous cofactors. This is not unexpected but variations will lead to artifactual differences. Neither quantitative nor qualitative differences could be detected between biopsies taken from healthy as compared to diseased individuals. No products other than PGE2, PGF2 alpha, TxB2, and 6-keto-PGF1 alpha (and metabolites thereof) could be demonstrated although special efforts were undertaken to determine whether there was any detectable lipoxygenase activity. Therefore it seems that future studies on the possible roles of prostaglandins in gastrointestinal physiology should be restricted to those compounds identified, primarily PGE2 and PGF2 alpha. The monotony in the pattern of products formed in homogenates from different tissues also suggests that in order to be able to detect possible differences between various conditions such studies should involve a minimum of tissue manipulation.

Adolescent↗

Lipoprotein abnormalities in patients with early primary biliary cirrhosis.

In twelve females with early forms of primary biliary cirrhosis (PBC) serum lipoproteins, the intravenous fat tolerance test ( IVFTT ) and the lecithin: cholesterol acyl transferase (LCAT) rate were determined and compared to healthy controls. The cholestatic LDL (LP-X) test was negative in all cases. PBC patients had lower very low density lipoprotein TG concentrations than controls and had levels of (high-density lipoprotein) HDL-TG, -cholesterol and -phospholipids that were about 50% higher than in controls. In PBC the HDL2-cholesterol concentration was double but the HDL3-cholesterol concentration was 60% of control values (P less than 0.001 for both). The LCAT rate and the IVFTT value did not differ between the groups. A typical finding on agarose gel electrophoresis was the appearance of a slow-moving alpha-band. Several interpretations of these results are possible. In PBC the hepatic lipase activity may be impaired leading to a shift of the HDL2/HDL3 relation. The transport of HDL2 to the liver lipase site may also be affected and HDL3 production reduced due to malabsorption in the intestine.

Adult↗

Prostaglandin E2 in basal gastric secretion and during stimulation of muscarinic receptors in man. Measurements with gas chromatography--mass spectrometry.

The physiological importance of prostaglandin E2 (PGE2) biosynthesis in the gastric mucosa is unknown. A role of endogenous prostaglandins in protecting the gastrointestinal epithelia has been suggested, but the evidence is insufficient and rarely supported by concomitant measurement of PG production. Amounts of PGE2 in luminal gastric contents which can be sampled atraumatically may reflect PGE2 synthesis in the gastric mucosa in vivo. To confirm earlier reported measurements made with radioimmunoassay we have measured by gas chromatography - mass spectrometry (GC-MS) PGE2 in gastric juice of five healthy men under basal conditions and during stimulation of muscarinic receptors with iv. bethanechol which in dog is reported to enhance PGE2 output. PGE2 was detected in all basal samples. The output was in median 32.1 pmol/15 min (range 17.0-105.4, 1 pmol = 0.352 ng), which is similar to results from earlier studies. Bethanechol infusion (60 micrograms . kg-1 . h-1) did not affect PGE2 outputs systematically in spite of a significant increase in outputs of acid and chlorides. Stimulation of muscarinic receptors does not seem to influence PGE2 synthesis in gastric mucosa in vivo. Alternatively changes in PGE2 synthesis may be masked by rapid chemical or enzymatical degradation or reabsorption of PGE2. Studies are under way to explore those phenomena.

Adult↗

Stimulation of gastric mucus output by somatostatin in man.

Effects of i.v. somatostatin on the gastric mucus output during a 60 min infusion of pentagastrin were examined in five healthy subjects. Experiments were also made with prior indomethacin administration to suppress the synthesis of endogenous prostaglandins. N-acetyl neuraminic acid, a sialic acid, was measured in the gastric aspirates as an index of gastric mucus. Somatostatin increased significantly the gastric mucus output in a dose-related way. The output increased to 158 +/- 14%, and 216 +/- 24% of the control level by 1 and 2 microgram kg-1h-1 somatostatin respectively. The increase induced by somatostatin was prevented by prior indomethacin. With indomethacin alone the mucus output was not different from in controls. Thus somatostatin has augmentory effects on the gastric mucus, which can be blocked by indomethacin, indicating that endogenous prostaglandins are involved in the augmentation. Somatostatin prevents stress ulcerations in the rat, assumedly by inhibiting the gastric acid secretion. This study suggests that additional mechanisms may contribute to the protective action of somatostatin on the gastric mucosa.

Adult↗

Sensitivity of the oxyntic and peptic cells to pentagastrin in duodenal ulcer patients and healthy subjects with similar secretory capacity.

The acid and pepsin responses to increasing doses of i.v. pentagastrin (0.01, 0.02, 0.1, 2.0 and 8.0 micrograms X kg-1 X h-1) were determined by gastric aspiration in 15 male duodenal ulcer (DU) patients and 11 male age-matched healthy controls (C). The lowest dose was infused for 60 min, the doses were then increased every 45 min. The stomach was continuously perfused with saline. Phenol red as marker showed an average loss of 8.4 +/- 1.4% in the DU and 10.0 +/- 1.4% in the C. Basal acid secretion and the dose-response (DR) curve for acid output (corrected for basal) did not differ for DU and C. The dose (D50) producing half the observed maximal acid response (MR), the calculated MR and calculated D50 was the same in DU and C. Similar results were obtained for pepsin secretion. The ratio of pepsin to acid secretion did not differ for DU and C. It is concluded that the sensitivity of the oxyntic as well as the peptic cells do not differ in DU and C with similar secretory capacity.

Adult↗

Serum and urinary bile acids in patients with primary biliary cirrhosis.

Serum concentrations and daily urinary excretions of unsulphated and total cholic (C) and chenodeoxycholic (CDC) acid were determined by radioimmunoassay in 15 patients with primary biliary cirrhosis. Thirteen patients had increased fasting serum bile acid concentrations; two of them had an increase of C only. An increase of C and CDC in serum was always followed by an increased urinary excretion of C and CDC. The individual serum bile acids were separated by gas-liquid chromatography. 3 beta-hydroxy-5-cholenoic acid was increased in nine patients, and its serum concentration was correlated to the total serum bile acid concentration. Deoxycholic (DC) and lithocholic (LC) acid were found in most patients, but their serum concentrations were not correlated to the total serum bile acid concentration. Minor bile acids comprised an average of 2% of the total concentration.

Adult↗

Measurements of prostaglandin biosynthesis in the gastrointestinal tract: biochemical and technical problems.

The special features of prostaglandin biochemistry, of importance for investigation of the possible physiological roles of prostaglandins, are briefly reviewed. The formation of prostaglandins and related compounds from endogenous and exogenous arachidonic acid in homogenates of human gastric mucosal and muscle-serosal layers is described. These preliminary data seem to indicate that a low conversion of exogenous precursor does not necessarily mean that the capacity of the tissue to synthesize prostaglandins from endogenous precursor is low.

Carbon Radioisotopes↗

Protection of the rat gastric mucosa by prostaglandin E2: possible relation to stimulation of the alkaline secretion.

Exogenous prostaglandins have specific protective effects on the gastric mucosa called cytoprotection which is proposed to be connected to the stimulatory effects of prostaglandins on the gastric nonparietal secretions. The protection by oral prostaglandin E2 (PGE2) against indomethacin-induced gastric erosions was studied in the rat, as was the effect on the protection of blocking the gastric alkaline secretion by acetazolamide. PGE2 reduced dose-dependently the indomethacin gastric erosion formation, confirming previous results from others. Acetazolamide caused very little damage when given alone but potentiated the indomethacin erosion formation in a dose-related way. PGE2 was less protective or without effect against lesions caused by indomethacin when given together with acetazolamide, but protection could be obtained by increasing the doses of PGE2. Indomethacin and acetazolamide are both blockers of the gastric bicarbonate secretion, which is stimulated by PGE2. The potentiation of indomethacin induced lesions by acetazolamide and the antagonistic actions between acetazolamide and PGE2 on mucosal protection are compatible with the hypothesis that stimulation of the alkaline secretion is one mechanism of cytoprotection of the gastric mucosa by PGE2.

Acetazolamide↗

Evaluation of fasting serum bile acid concentration in patients with liver and gastrointestinal disorders.

Fasting concentrations of S-cholate, S-chenodeoxycholate, S-aminotransferases, S-bilirubin, S-alkaline phosphatases, and S-glutamyltransferase were determined in 564 outpatients with disorders of the liver and gastrointestinal tract. Unsulphated conjugates of cholic (fS-C) and chenodeoxycholic acid (fS-CDC) were determined by radioimmunoassay. In patients with increased serum bile acid concentrations fS-C and fS-CDC were linearly correlated, and the fS-C/fS-CDC ratio was similar in all patient groups. The incidence of false-positive results of fS-CDC was probably due to inadequate fasting and comparison of fS-C only with the liver tests. In 51 patients with verified cirrhosis fS-C was significantly correlated with S-bilirubin in a semilogarithmic relation but not with S-alkaline phosphatases or S-glutamyltransferase. fS-C was found to be a sensitive indicator of liver disease in the anicteric stage. Of 207 patients with inflammatory bowel disease, 63 had 1 or several of the results of liver tests for cholestasis elevated. There was no correlation between the different tests. In these patients and all patients with gastrointestinal disorders the commonest single finding was an elevation of S-alkaline phosphatases not associated with cholestasis.

Bile Acids and Salts↗

Acetazolamide interferes with the protective effect of prostaglandin E2 in the rat gastric mucosa.

Oral prostaglandin E2 protected the gastric mucosa against the damage induced by intraperitoneal indomethacin in the rat. Blocking of the gastric alkaline secretion by subcutaneous acetazolamide potentiated the ulcerogenic action of indomethacin and reduced or abolished the protective effect of a submaximal dose prostaglandin E2. The results are compatible with the hypothesis that stimulation of the alkaline secretion is one of the mechanisms by which prostaglandin E2 protects the gastric mucosa.

Acetazolamide↗