Role of gastric acid inhibition, prostaglandins and endogenous-free thiol groups on the gastroprotective effect of a proteolytic fraction from V asconcellea cundinamarcensis latex

2014 ◽  
Vol 67 (1) ◽  
pp. 133-141 ◽  
Author(s):  
Ana Candida Araujo e Silva ◽  
Fernanda de Oliveira Lemos ◽  
Marco Túlio Ribeiro Gomes ◽  
Carlos Edmundo Salas ◽  
Miriam Teresa Paz Lopes
Keyword(s):  
Gastric Acid ◽  
Acid Inhibition ◽  
Thiol Groups ◽  
Free Thiol ◽  
Gastroprotective Effect ◽  
Gastric Acid Inhibition

Effect of gastrin on antroduodenal motility: role of intraluminal acidity

1998 ◽  
Vol 275 (5) ◽  
pp. G1209-G1216 ◽  
Author(s):  
M. Verkijk ◽  
H. A. J. Gielkens ◽  
C. B. H. W. Lamers ◽  
A. A. M. Masclee
Keyword(s):  
Gastric Acid ◽  
Healthy Subjects ◽  
Cycle Length ◽  
Potential Effect ◽  
Acid Inhibition ◽  
Phase Iii ◽  
Gastric Acid Inhibition ◽  
Antroduodenal Manometry ◽  
Antroduodenal Motility

The effect of gastrin on the migrating motility complex (MMC) was studied in seven healthy subjects. It was hypothesized that a potential effect of gastrin on the MMC may result from intraluminal acidification through increased gastric acid secretion. Therefore, antroduodenal manometry and intraluminal acidity were recorded simultaneously. The effect of gastric acid inhibition, with and without administration of gastrin, on antroduodenal motility and intraluminal acidity was also evaluated and compared with saline infusion (control). Continuous infusion of gastrin-17 (20 pmol ⋅ kg−1⋅ h−1) increased intragastric and intraduodenal acidity and suppressed phase II and phase III motor activity in both antrum and duodenum. Concomitant gastric acid inhibition with intravenous famotidine, as demonstrated by intragastric neutralization of pH, completely antagonized the effect of gastrin on the MMC. In fact, famotidine infusion, both with and without administration of gastrin, significantly shortened MMC cycle length. It is concluded that the effect of gastrin on interdigestive antroduodenal motility results from increased intraluminal acidity.

Comparison of lansoprazole and famotidine on gastric acid inhibition during daytime and nighttime in different CYP2C19 genotype groups

2001 ◽  
Vol 120 (5) ◽  
pp. A433
Author(s):  
Naohito Shirai ◽  
Takahisa Furuta ◽  
Fang Xiao ◽  
Masayoshi Kajimura ◽  
Hiroyuki Hanai
Keyword(s):  
Gastric Acid ◽  
Acid Inhibition ◽  
Cyp2c19 Genotype ◽  
Gastric Acid Inhibition

scholarly journals Reassessment of Gastric Acid Inhibition by Cyholecystokinin and Gastric Inhibitory Polypeptide in Dogs

1982 ◽  
Vol 83 (5) ◽  
pp. 1047-1050 ◽  
Author(s):  
Emeran A. Mayer ◽  
Janet Elashoff ◽  
Viktor Mutt ◽  
John H. Walsh
Keyword(s):  
Gastric Acid ◽  
Gastric Inhibitory Polypeptide ◽  
Acid Inhibition ◽  
Gastric Acid Inhibition

Efficiency of Potent Gastric Acid Inhibition

Drugs ◽  
2005 ◽  
Vol 65 (Supplement 1) ◽  
pp. 105???111 ◽  
Author(s):  
Fernando Carballo
Keyword(s):  
Gastric Acid ◽  
Acid Inhibition ◽  
Gastric Acid Inhibition

scholarly journals Acid inhibition by intestinal nutrients mediated by CCK-A receptors but not plasma CCK

2001 ◽  
Vol 281 (4) ◽  
pp. G924-G930 ◽  
Author(s):  
K. C. Kent Lloyd ◽  
Jiafang Wang ◽  
Travis E. Solomon
Keyword(s):  
Acid Secretion ◽  
Gastric Acid ◽  
Trypsin Inhibitor ◽  
Acid Output ◽  
Liquid Diet ◽  
Acid Inhibition ◽  
Soybean Trypsin Inhibitor ◽  
The Individual

We examined the role of CCK-A receptors in acid inhibition by intestinal nutrients. Gastric acid and plasma CCK and gastrin levels were measured in rats with gastric and duodenal fistulas during intragastric 8% peptone and duodenal perfusion with saline, complete liquid diet (CLD; 20% carbohydrate, 6% fat, and 5% protein), and the individual components of CLD. Acid output was significantly inhibited (50–60%) by CLD, lipid, and dextrose. Plasma CCK was significantly increased by CLD (from 2.6 ± 0.3 to 4.8 ± 0.5 pM) and lipid (4.6 ± 0.5 pM). CCK levels 50-fold higher (218 ± 33 pM) were required to achieve similar acid inhibition by exogenous CCK-8 (10 nmol · kg−1 · h−1 iv). Intestinal soybean trypsin inhibitor elevated CCK (10.9 ± 2.5 pM) without inhibiting acid secretion. The CCK-A antagonist MK-329 (1 mg/kg iv) reversed acid inhibition caused by CLD, lipid, and dextrose. Peptone-stimulated gastrin (21.7 ± 1.9 pM) was significantly inhibited by CLD (14.5 ± 3.6 pM), lipid (12.3 ± 2.2 pM), and dextrose (11.9 ± 1.5 pM). Lipid and carbohydrate inhibit acid secretion by activating CCK-A receptors but not by altering plasma CCK concentrations.

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