Non-steroidal anti-inflammatory drugs and prostaglandin effects on pepsinogen secretion by dispersed human peptic cells.

Lanas, Ángel; Nerín, J.; Esteva, Francisco J.; Sainz, Ricardo Calle

doi:10.1136/gut.36.5.657

Cited by 9 publications

(4 citation statements)

References 30 publications

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“…It must be said that none of the assayed NSAIDs at the concentrations used significantly modified the percentage of glandular cells that excluded the trypan blue stain or the amount of lactate dehydrogenase and phosphoglucose isomerase released into the incubation medium. Our results confirm previous findings (13,23,43) and indicate that the concentrations of NSAIDs used in this study did not affect the cellular integrity of gastric glands.…”

Section: Discussionsupporting

confidence: 95%

Inhibition of acid secretion by the nonsteroidal anti-inflammatory drugs diclofenac and piroxicam in isolated gastric glands: analysis of a multifocal mechanism

Salvatella¹,

Rossi²,

Valle³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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In nonstimulated rabbit gastric glands, acetylsalicylic acid (10-500 microM) and indomethacin (3-300 microM) did not significantly modify the basal rate of acid secretion, whereas diclofenac and piroxicam (10-1,000 microM each) caused a marked and dose-dependent inhibitory effect (EC(50) = 138 and 280 microM, respectively). In gastric glands stimulated by histamine (100 microM), diclofenac also reduced the rate of acid formation in a dose-dependent manner. In contrast, acetylsalicylic acid, indomethacin, and piroxicam exerted a biphasic effect; thus low concentrations (3-100 microM) of these three agents significantly increased the rate of histamine-stimulated acid secretion (10-20% over the corresponding control value) by a cAMP-independent mechanism, whereas higher concentrations reduced the rate of acid formation. With respect to underlying biochemical mechanisms that could mediate inhibitory effects of NSAIDs on gastric acid formation, it was observed that both diclofenac and piroxicam, but not acetylsalicylic acid or indomethacin, decreased the glandular content of ATP, inhibited hydrolytic activity of gastric gland microsomal H(+)-K(+)-ATPase, and reduced the rate of H(+)-K(+)-ATPase-dependent proton transport across microsomal membranes in a dose-dependent manner. Furthermore, diclofenac and piroxicam also significantly increased passive permeability of microsomal membranes to protons. In conclusion, our work shows that diclofenac and piroxicam cause a significant reduction in the rate of basal and histamine-stimulated acid formation in isolated rabbit gastric glands at concentrations that can be attained in the gastric lumen of patients treated with these drugs. Mechanisms involved in these inhibitory effects appear to be multifocal and include different steps of stimulus-secretion coupling.

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Section: Discussionsupporting

confidence: 95%

Inhibition of acid secretion by the nonsteroidal anti-inflammatory drugs diclofenac and piroxicam in isolated gastric glands: analysis of a multifocal mechanism

Salvatella¹,

Rossi²,

Valle³

et al. 2004

American Journal of Physiology-Gastrointestinal and Liver Physi

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“…An aliquot of the supernatant was assayed for pepsinogen activity using a modified Anson-Mirsky method using acid denatured haemoglobin as the substrate, as previously described. 16 Secretory responses to stimuli were calculated as output per unit time with basal output subtracted. Mean (SEM) basal rate of pepsinogen secretion in the experiments was 0.18% (0.007) of total pepsinogen content per minute.…”

Section: Experiments and Calculationsmentioning

confidence: 99%

Helicobacter pylori stimulates pepsinogen secretion from isolated human peptic cells

Lorente

Doiz²,

Serrano³

et al. 2002

Gut

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Background: Different acid and peptic related gastroduodenal diseases are associated with both increased gastric secretion and Helicobacter pylori infection. Patients with H pylori associated gastritis or duodenal ulcer have increased serum pepsinogen levels which decrease after eradication. The mechanisms of H pylori induced gastric mucosal damage are not completely understood. Aim: To determine the effects of H pylori on pepsinogen secretion from isolated human peptic cells. Methods: Dispersed human peptic cells were prepared from endoscopically obtained biopsy specimens after collagenase digestion, mechanical disruption, and density gradient centrifugation. H pylori was obtained from gastric biopsies (antrum and body), and cultured in non-selective and selective media. Isolates of H pylori were used at different concentrations (1-20×10 6 colony forming units (cfu)).Results: H pylori (10

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“…The NSAID-induced upper gastrointestinal injury results from both local effects and systemic prostaglandin inhibition effected by blocking cyclooxygenase-1 [12]. Consequently, many efforts were made for discovering selective cox-2 inhibitors.…”

Section: Discussionmentioning

confidence: 99%

The Incidence of Upper Gastrointestinal Complications of Non-Steroidal Anti-Inflammatory Drugs in Elderly Patients

Hassanein¹,

Abdelrahim²,

Said³

et al. 2014

Med-Science

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Non-steroidal anti-inflammatory drugs and prostaglandin effects on pepsinogen secretion by dispersed human peptic cells.

Cited by 9 publications

References 30 publications

Inhibition of acid secretion by the nonsteroidal anti-inflammatory drugs diclofenac and piroxicam in isolated gastric glands: analysis of a multifocal mechanism

Inhibition of acid secretion by the nonsteroidal anti-inflammatory drugs diclofenac and piroxicam in isolated gastric glands: analysis of a multifocal mechanism

Helicobacter pylori stimulates pepsinogen secretion from isolated human peptic cells

The Incidence of Upper Gastrointestinal Complications of Non-Steroidal Anti-Inflammatory Drugs in Elderly Patients

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