Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Published data show that smokers have greater basal or peak acid and pepsin outputs, but the mechanisms underlying these effects are unknown. To confirm this and to determine whether these findings extend to, and implicate, any vagal overactivity, gastric secretions collected for 1 h basally, 1 h after 15 min of modified sham feeding (MSF), and 1 h after pentagastrin (6 micrograms/kg subcutaneously) were analyzed for acid and pepsin content in 204 subjects, 104 with duodenal ulcer (66 smokers) and 101 without (57 smokers). Maximal acid outputs (MAO, mu eq/kg/h, means +/- SEM) were higher in smokers than in non-smokers in both duodenal ulcer (DU) (623 +/- 35 versus 491 +/- 35, p less than 0.005) and non-DU (502 +/- 32 versus 376 +/- 20, p less than 0.005). Basal and MSF secretions were generally increased in smokers but, when expressed as a percentage of MAO, were not different in smokers and non-smokers (18% versus 17% and 43% versus 39%, respectively, in DU, and 13% versus 16% and 40% versus 36% in non-DU). Maximal pepsin outputs (units x 10(-2)/kg/h) were also higher in smokers than in non-smokers (DU, 129 +/- 7.9 versus 105 +/- 9.5, p = 0.05, and non-DU, 101 +/- 7.5 versus 77 +/- 10, p = 0.05). Basal and MSF secretions as a percentage of maximal pepsin output were not different in smokers versus non-smokers. Multivariate logistic regression shows that smoking was most strongly associated with MAO and sham feeding outputs, but the duration-intensity (pack-years) of smoking was associated only with elevated MAO.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Influence of smoking on basal and on vagally and maximally stimulated gastric acid and pepsin secretion. 150 83

The commonly accepted model for gastric emptying suggests that the 'antral mill' is responsible for the triturition and subsequent emptying of solid food from the stomach. Little is known about the contribution to solid emptying made by other digestive mechanisms such as acid-pepsin secretion. We have investigated the effect of inhibiting gastic secretion on the rate at which a solid test meal emptied from the stomach. Using a radiolabelled beefburger, we performed paired gammacamera studies on consecutive days in 10 fasted, healthy volunteers to compare gastric emptying of the test meal with and without oral cimetidine (400 mg 1 hour before the test, 800 mg at the start of the meal). Inhibition of acid-pepsin secretion by cimetidine was associated with an appreciable delay in the rate of emptying of the burger from the stomach (T50 cimetidine 187 (16) min (mean (SEM); T50 no cimetidine 146 (15) min; p less than 0.01, paired t test). This delay was related to a change in the slope of the emptying profile and was not associated with a prolonged lag phase. These results may be explained by the relative achlorhydria and reduced pepsin activity induced by cimetidine impairing the breakdown of solid food into particles small enough to leave the stomach.
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PMID:Influence of acid-pepsin secretion on gastric emptying of solids in humans: studies with cimetidine. 175 58

Microdissection of acellular rat renal cortex with pepsin was carried out to investigate the morphological substructure of glomerular basement membrane (GBM) by high resolution SEM. Renal cortical blocks (less than 5 mm3) from adult male Sprague Dawley rats were rendered acellular by sequential detergent extraction and digested up to 184 hrs with 5 mg/ml pepsin (185 U/mg) in 0.5 M acetic acid (pH 2) at 10-15 degrees C. Samples were conventionally prepared for SEM, and observed at original magnifications of 500-100,000 diameters. At low magnifications (500-5,000x), acellular GBM surfaces appeared smooth at all digestion times. At higher magnifications (50,000-100,000x), control GBM surfaces were finely granular. Granule diameter ranged from 20-80 nm, with most between 30-40 nm. Pepsin digestion did not affect average granule size. Beginning at 44 hrs of digestion, intrinsic fibrillar structures comprised of linear arrays of 20-40 nm granules were observed on/in GBM surfaces. At later incubation times, this component of GBM became more extensive. At 160 hrs, the fibrillar arrays frequently bifurcated and showed distinctive "forked" termini, some of which comprised two sides of a triangle (120-150 nm on a side). Fork "handles" (310-350 nm in length) radiated from each angle of the triangle. These sometimes terminated in large granules (approximately 100 nm in diameter), two of which appeared to connect fibrillar arrays end-to-end. Together with other arrays, the interconnected triangles appeared to comprise a three-dimensional meshwork extending into the GBM and possibly providing support for, its granular components.
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PMID:High resolution SEM analysis of acellular glomerular basement membrane following pepsin digestion: intrinsic fibrillar structures. 213 83

The role of the lateral hypothalamic area (LHA) in the development of gastric mucosal damages induced by water immersion restraint stress was evaluated in bilateral LHA-lesioned rats. The ulcer index of lesions (M +/- SEM, mm) was significantly higher in LHA-lesioned rats (21.6 +/- 2.8) than in both thalamus-lesioned rats (9.8 +/- 2.0) and non-treated rats (10.2 +/- 1.5). The gastric acid and pepsin outputs during water immersion for 5 hours were significantly lower in the LHA-lesioned rats than in both the control rats. In the LHA-lesioned rats, PAS-positive mucus content of gastric corpus without lesions was significantly decreased after water immersion restraint stress for 5 hours. All these results suggest that lateral hypothalamic area plays an important role in the process of stress ulcer formation mainly through the disturbance of mucosal defensive mechanism such as changes in gastric mucus contents.
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PMID:[Effect of the lateral hypothalamic area-lesions on the development of gastric mucosal damages by water immersion restraint stress in rats]. 221 61

The effect of the H2 agonist impromidine, gastrin 1-17 (G1-17), pentagastrin, and the M1 agonist McN-A-343 on pepsin secretion in the acid-inhibited totally isolated, vascularly perfused rat stomach was studied. Omeprazole produced a 97-98% inhibition of stimulated acid outputs. Base-line pepsin output after omeprazole was 712 +/- 278 micrograms/h (mean +/- SEM) and, after stimulation with impromidine, 1528 +/- 164 micrograms/h; G1-17, 1520 +/- 180 micrograms/h; and pentagastrin, 2063 +/- 605 micrograms/h. Output after McN-A-343 was 534 +/- 69 micrograms/h. Pepsin secretion after impromidine, G1-17, and pentagastrin was significantly (p less than 0.01) higher than base-line output. McN-A-343 had no significant effect on pepsin output in this model. Pepsin secretion after impromidine, G1-17, and pentagastrin was considerably lower than found in the same model with uninhibited acid output. This could be caused by decreased tubular 'washout' after acid inhibition, and, accordingly, no conclusions can be drawn as to the possible stimulatory effect of acid on pepsin secretion. However, the present study indicates that pepsin secretion can be stimulated directly by impromidine and (penta)gastrin without concomitant acidification of the gastric glands.
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PMID:Stimulated pepsin secretion after omeprazole-induced acid suppression in the totally isolated, vascularly perfused rat stomach. 243 47

Normal human B cell proliferation is controlled by various immunoregulatory signals including the T cell-derived lymphokine B cell growth factor (BCGF). Human BCGF provides the final proliferative signal to normal, activated B cells. We herein show that anti-CR2 monoclonal antibodies inhibit human B cell responsiveness to purified BCGF. Addition of anti-CR2 antibody, AB5, was capable of completely inhibiting BCGF-mediated enhancement of either anti-mu or staphylococcal protein A-activated human B cells (191 +/- 21 cpm vs. 3942 +/- 622 cpm, mean +/- SEM). Inhibition of B cell response to BCGF by AB5 occurred in a dose-dependent manner. Monoclonal antibody anti-B2, which recognizes the same 140-kDa glycoprotein as AB5, in comparable concentrations also inhibited B cell responsiveness to BCGF. Monoclonal antibodies of the same subclass (IgG1) showed no inhibitory effect on BCGF enhancement of B cell proliferation. The F(ab')2 fragment of AB5 generated by pepsin digestion was similarly inhibitory as was the intact Ig. AB5-mediated inhibition was independent of the target B cell state of activation. Both resting and activated B cells (anti-mu or staphylococcal protein A activated) incubated with similar concentrations of AB5 were unresponsive to BCGF. The ability of anti-CR2 antibodies to block BCGF-dependent B cell proliferation suggests that occupancy of C3d membrane receptors may result in modulation of B cell proliferation in physiologic or clinical disease states.
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PMID:Inhibition of B cell growth factor (BCGF) by monoclonal antibodies directed against the C3d receptor (CR2). 293 67

The effect of peptide YY (PYY) on gastric and pancreatico-biliary secretion was studied in humans. Peptide YY was infused into groups of 6 healthy volunteers at doses of 0.59, 0.20, and 0.064 pmol X kg-1 X min-1. The two higher doses caused a significant suppression of gastric acid and pepsin output during background stimulation with pentagastrin. The middle dose of PYY (0.20 pmol X kg-1 X min-1) that increased plasma PYY levels by 27 +/- 2 pM caused a 90% +/- 18% (mean +/- SEM; p less than 0.001) reduction in the incremental gastric volume response to pentagastrin. Similarly this dose of PYY caused a substantial inhibition of the acid (77% +/- 14%; p less than 0.005) and pepsin (96% +/- 22%; p less than 0.01) response to pentagastrin; in 2 subjects, pepsin output fell to below basal levels. In contrast, the highest dose of PYY (0.62 pmol X kg-1 X min-1) had no significant influence on duodenal juice volume, output of bicarbonate, trypsin, or bilirubin during low dose stimulation with secretin (0.25 pmol X kg-1 X min-1) and cholecystokinin-8 (0.15 pmol X kg-1 X min-1). Thus PYY concentrations in the circulation similar to those seen after the ingestion of food cause a marked reduction in gastric secretion. This peptide should therefore be considered as one of the possible candidates for the classical enterogastrone.
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PMID:Effect of peptide YY on gastric, pancreatic, and biliary function in humans. 383 79

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.
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PMID:Acid instillation increases gastric luminal prostaglandin E2 output in man. 386 36

The regulation of pepsin secretion was studied in the in vitro perfused mouse stomach. In contrast to acid secretion, basal pepsin release was not inhibited by 10(-4) M carbonyl cyanide m-chlorophenylhydrazine (CCCP) and by N2-induced hypoxia. Both secretions were not affected by 10(-3) M cimetidine, 10(-3) M atropine or cycloheximide (2 mg i.p. + 10(-5) M). Secretory responses to classical stimulants were similar to those obtained under in vivo conditions: carbamylcholine (CCH) and histamine stimulated acid and pepsin secretion in parallel, with a maximal pepsin/acid ration of 34 +/- 4 (mean +/- SEM) and 40 +/- 5, respectively. CCH-induced pepsin secretion was inhibited by atropine and pirenzepine. Dibutyrylic cyclic AMP(db-cAMP) strongly stimulated pepsin release. This stimulation was partially inhibited by trifluoperazine. Pentagastrin was a weak stimulant of pepsin secretion (pepsin/acid ratio: 10 +/- 3), whereas 10(-4) M bombesin and 10(-6) M salmon calcitonin had no effect. Omeprazole (H168/68) strongly inhibited basal acid secretion and stimulated pepsin release in a dose-and energy-dependent fashion. In contrast to acid, basal pepsin release probably represents an 'overflow secretion'. Although pepsin and acid are usually stimulated in parallel, dissociated responses are obtained under in vitro conditions, indicating that separate regulatory pathways exist.
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PMID:Pepsin secretion: neurohumoral regulation and drug effects. 610 Jun 25

The effect of an oral therapeutic dose of 150 mg of ranitidine on the acid and pepsin response to sham feeding and pentagastrin was examined in healthy volunteers, using a double-blind random-isation method. Gastric juice was collected up to 255 minutes after ingestion of the drug. In placebo-treated subjects, basal acid secretion rate and the secretion rate following sham feeding and injection of 6 micrograms/kg of pentagastrin were 5.3 meq/h +/- 2.0 SEM, 12.3 +/- 3.2, and 24.4 +/- 5.4, respectively. The corresponding values in ranitidine-treated subjects were 0.1 +/- 0.1, 0.5 +/- 0.2, and 3.4 +/- 1.2, respectively. The reduction of acid secretion in all three instances is statistically significant (p less than 0.025, p less than 0.05, and p less than 0.05, respectively). Basal, sham feeding-stimulated, and pentagastrin-stimulated pepsin secretion rates in the placebo-treated group were 38.4 mg/h +/- 7.0 SEM, 68.6 +/- 13.2, and 39.2 +/- 8.0, respectively. In the ranitidine-treated group, the values were 5.0 +/- 3.4, 13.2 +/- 5.6, and 19.6 +/- 5.0, respectively. The reduction of pepsin secretion during basal state and following sham feeding is statistically significant (p less than 0.005 and p less than 0.01). Thus, oral ranitidine inhibits the acid and pepsin response to sham feeding in man. Its inhibitory effect on the acid response to pentagastrin lasts for at least 4 hours.
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PMID:Ranitidine inhibits gastric acid and pepsin secretion following sham feeding. 611 Jun 26


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