Mechanism of Stress Ulcer: Influence of Hypovolemic Shock on Energy Metabolism in the Gastric Mucosa

Menguy, René; Desbaillets, L.; Masters, Y. F.

doi:10.1016/s0016-5085(74)80077-6

Cited by 161 publications

(30 citation statements)

References 6 publications

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“…An energy deficit has been considered to be a pathogenic factor in ulcerative colitis, which is substantiated by the fact that the intestinal mucosa has a limited capacity for de novo synthesis of purine nucleotides [17] and is more prone to reduced ATP concentrations compared with the liver or muscle [18]. On the other hand, IL-6 and tumor necrosis factor α (TNF-α) has been shown to play an important role in the pathogenesis of inflammatory bowel disease [19].…”

Section: Introductionmentioning

confidence: 99%

Protective effects of N-acetylcysteine on acetic acid-induced colitis in a porcine model

Wang

Hou

et al. 2013

BMC Gastroenterol

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BackgroundUlcerative colitis is a chronic inflammatory disease and involves multiple etiological factors. Acetic acid (AA)-induced colitis is a reproducible and simple model, sharing many characteristics with human colitis. N-acetylcysteine (NAC) has been widely used as an antioxidant in vivo and in vitro. NAC can affect several signaling pathways involving in apoptosis, angiogenesis, cell growth and arrest, redox-regulated gene expression, and inflammatory response. Therefore, NAC may not only protect against the direct injurious effects of oxidants, but also beneficially alter inflammatory events in colitis. This study was conducted to investigate whether NAC could alleviate the AA-induced colitis in a porcine model.MethodsWeaned piglets were used to investigate the effects of NAC on AA-induced colitis. Severity of colitis was evaluated by colon histomorphology measurements, histopathology scores, tissue myeloperoxidase activity, as well as concentrations of malondialdehyde and pro-inflammatory mediators in the plasma and colon. The protective role of NAC was assessed by measurements of antioxidant status, growth modulator, cell apoptosis, and tight junction proteins. Abundances of caspase-3 and claudin-1 proteins in colonic mucosae were determined by the Western blot method. Epidermal growth factor receptor, amphiregulin, tumor necrosis factor-alpha (TNF-α), and toll-like receptor 4 (TLR4) mRNA levels in colonic mucosae were quantified using the real-time fluorescent quantitative PCR.ResultsCompared with the control group, AA treatment increased (P < 0.05) the histopathology scores, intraepithelial lymphocyte (IEL) numbers and density in the colon, myeloperoxidase activity, the concentrations of malondialdehyde and pro-inflammatory mediators in the plasma and colon, while reducing (P < 0.05) goblet cell numbers and the protein/DNA ratio in the colonic mucosa. These adverse effects of AA were partially ameliorated (P < 0.05) by dietary supplementation with NAC. In addition, NAC prevented the AA-induced increase in caspase-3 protein, while stimulating claudin-1 protein expression in the colonic mucosa. Moreover, NAC enhanced mRNA levels for epidermal growth factor and amphiregulin in the colonic mucosa.ConclusionDietary supplementation with NAC can alleviate AA-induced colitis in a porcine model through regulating anti-oxidative responses, cell apoptosis, and EGF gene expression.

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Section: Introductionmentioning

confidence: 99%

Protective effects of N-acetylcysteine on acetic acid-induced colitis in a porcine model

Wang

Hou

et al. 2013

BMC Gastroenterol

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“…In vivo the 2 interactions that occur within the therapeutic range of free aspirin (0.15 to 0.6 mmol/L) are mitochondrial uncoupling and inhibition of protein synthesis, possibly by action on the endoplasmic reticulum (Smith & Dawkins 1971) though there may be a more specific effect of aspirin in the inhibition of expression of mRNA for cyclo-oxygenase (Sanduja et al 1990). Menguy et al (1974) examining the effect of hypovolaemic shock on energy metabolism showed that the onset of gastric ulceration coincided with a profound drop in intracellular A TP concentration. This was associated with a fall in transmucosal potential difference and increased permeability.…”

Section: Direct Cellular Toxicitymentioning

confidence: 99%

Gastroprotection and Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

Hayllar

Bjarnason

1992

Drug Safety

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There is no doubt that nonsteroidal anti-inflammatory drugs (NSAIDs) cause gastrointestinal injury. The most serious consequences are gastric and duodenal ulcers which can cause bleeding and perforation, and which may lead to the premature death of 3000 to 4000 patients in the UK annually. The immediate actions of NSAIDs operate at a subcellular level; in particular altering of mitochondrial function which causes depletion of ATP and renders the cell vulnerable to oxidant stress. Secondary consequences follow, such as the inhibition of prostaglandin synthesis which delays cellular repair. While adaptation can be shown in volunteers despite continued NSAID ingestion, studies in patients suggest mucosal damage develops continuously and cumulatively even with low doses of aspirin. Histamine H2-receptor antagonists and proton pump inhibitors heal NSAID-related ulcers, though healing rates with H2-antagonists are slower in patients who continue NSAID treatment. They have little role in preventing damage. In addition to acid suppression, prostaglandin analogues cause bicarbonate secretion and enhance mucosal blood flow. They have a specific role in both prevention and treatment of NSAID-related damage. The use of misoprostol offers a rational approach to reduce the high prevalence of unwanted gastroduodenal damage from NSAIDs. On a purely financial basis more information is needed before routine coprescribing can be recommended. However, for any patient on NSAIDs with a previous ulcer or for patients aged over 60 years (where the risks and seriousness of complications are markedly increased), the use of misoprostol should be considered. Further developments in prostaglandin analogues may reduce their adverse effects and perhaps thereby improve their efficacy at symptom control.

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“…The presence of tissue hypoxia has been suggested as one of the main causative factors in the development of gastric mucosal injury (in acute ulcer phase and in other injuries in later phase) based on widely performed physiological blood flow observations. 1–4 …”

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confidence: 99%

“…Based on the observations of Menguy et al , 1–4 experimental and clinical researchers have generally accepted that a strong correlation exists between a decrease in gastric mucosal blood flow and a decrease in gastric mucosal ATP levels as a consequence of tissue hypoxia in the gastric mucosa (without any scientifically proven arguments). It is very important to emphasize that the observations of Menguy et al were carried out in rats subjected to haemorrhagic shock and that ATP in the gastric fundus decreased by 67%, but only decreased by 23% in the antrum.…”

mentioning

confidence: 99%

“…It is very important to emphasize that the observations of Menguy et al were carried out in rats subjected to haemorrhagic shock and that ATP in the gastric fundus decreased by 67%, but only decreased by 23% in the antrum. 1–4 All other reports that have dealt with tissue hypoxia versus tissue ATP in gastrointestinal mucosa have cited the results of Menguy et al as a key argument in their different experiments and clinical observations. There is no question that in the work by Menguy et al , ATP resynthesis (by way of impaired oxidative phosphorylation) was limited by the haemorrhagic shock induced in the experiments.…”

mentioning

confidence: 99%

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Membrane‐bound, ATP‐dependent energy systems and tissue hypoxia in human gastric mucosa

Mózsik

Figler

Rumi

2000

J of Gastro and Hepatol

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Mechanism of Stress Ulcer: Influence of Hypovolemic Shock on Energy Metabolism in the Gastric Mucosa

Cited by 161 publications

References 6 publications

Protective effects of N-acetylcysteine on acetic acid-induced colitis in a porcine model

Protective effects of N-acetylcysteine on acetic acid-induced colitis in a porcine model

Gastroprotection and Nonsteroidal Anti-Inflammatory Drugs (NSAIDs)

Membrane‐bound, ATP‐dependent energy systems and tissue hypoxia in human gastric mucosa

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