Prostaglandins and Peptic Ulcer Therapy

Walt, R P

doi:10.3109/00365529009091927

Cited by 15 publications

(4 citation statements)

References 47 publications

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“…Adults with peptic ulcer disease, especially during treatment with nonsteroidal antiinflammatory drugs, can be treated with dPGE2 (Arbocet; Upjohn, Kalamazoo, MI) (13,29). However, our present data suggest that there may be an age-related delay in the protective effects of dPGE2.…”

Section: Discussioncontrasting

confidence: 54%

Developmental Changes in Gastric Mucus Gel Thickness: Responsiveness to 16,16-Dimethyl Prostaglandin E2 and Mucosal Protection in the Rat

et al. 1992

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ABSTRACT. The gastric mucosa of newborn rats is sen-there may be some deficiency in defensive factors that predispose sitive to the damaging effects of acid and ethanol. We neonates to mucosal injury. measured gastric mucus gel thickness in newborn, suckling,In this study, we investigated age-related changes in mucus and weaned rats by inversion microscopic observation. The layer thickness and its responsiveness to PG in developing rats. thickness in newborn rats was 52.2 2 6.7 pm and increased We also studied the effect of PG on ethanol-induced gastric with age, reaching 96.8 f 5.6 pm in 8-wk-old rats (p < mucosal damage, using PG doses identical to those used to test 0.001). Oral administration of 16,16-dimethyl prostaglan-mucus thickness. din Ez at concentrations of 10 and 100 pg/kg body weight increased mucus thickness in 8-wk-old rats but had no effect in 1-wk-old rats. We also assessed the effect of MATERIALS AND METHODS 16,16-dimethyl prostaglandin E2 on the prevention of gastric mucosal damage induced by ethanol. Oral 16,16-diMeasurement of mucus gel layer thickness. Newborn (3 d), methyl prostaglandin E2 reduced damage in &wk-old rats, suckling (1 and 2 wk), and weaned (4 and 8 wk) Wistar rats were but there was no effect in 1-wk-old rats. These data suggest used. They were fasted 30-36 h (3-d-and I-and Zwk-old rats) that the susceptibility of newborn rats to gastric mucosal or 40-48 h (4-and 8-wk-old rats). Water was allowed ad libitum injury may be related to the relative thinness of the gastric until 30-36 h before the rats were killed. Preliminary studies mucus gel layer and the failure of prostaglandins to in-showed that those time intervals are the shortest times that insure crease the mucus gel layer thickness. (Pediatr Res 31: stomachs empty of food. Preliminary studies also showed that 193-195,1992) the mucus gel thickness in newborn rats given water containing 0.3% NaCl and 5% glucose every 12 h before death was not Abbreviations significantly different from the thickness in the newborn rats that were not given the solution. Newborn and suckling rats were put PG, prostaglandin in a box. Half of the bottom of the box was warmed to 37-4O0C, dPGE2, 16,16-dimethyl prostaglandin Ez and half was at room temperature (25°C). Rats were free to choose a position in the box. Twenty-four h before study, weanling rats were placed in cylindrical wire mesh cages to prevent coprophagy. Rats were killed by intrathecal or intraperitoneal injection of pentobarbital after a light ether anesthesia. Gastroduodenal mucosal lesions are relatively frequent inThe method reported by Kerss et al.( 1 9) was used with slight neonates (1-3) and may cause serious bleeding. The gastric modifications to measure surface mucus thickness. The stomach mucosa of newborn rats is more susceptible to injury after was removed and opened along the lesser curvature. The tissue, intragastric ingestion of HCl(4) and ethanol (5) than the mucosa luminal surface up, was mounted on a filter paper (Whatman of adult rats. Gastric mucosal lesions...

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Section: Discussioncontrasting

confidence: 54%

Developmental Changes in Gastric Mucus Gel Thickness: Responsiveness to 16,16-Dimethyl Prostaglandin E2 and Mucosal Protection in the Rat

et al. 1992

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“…Two analogues, misoprostol and enprostil, are currently being marketed for peptic ulcer disease and are the most widely used (Walt 1990). Enprostil is a synthetic prostaglandin E2 analogue with similar properties to misoprostol (Aly 1987).…”

Section: Prostaglandin Analoguesmentioning

confidence: 98%

Renal Effects of Peptic Ulcer Therapy

Burgess

Muruve

1992

Drug Safety

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Drugs used in the treatment of peptic ulcer disease may interact with the renal system in a variety of ways. Since many agents are eliminated by renal excretion, clearance of these agents may be reduced and half-life extended in the presence of renal insufficiency. The histamine H2-receptor antagonists may interfere with renal tubular excretion of creatinine and cationic drugs, resulting in elevated serum concentrations and reduced renal clearance. The prostaglandin E1 analogue misoprostol is used as a cytoprotective agent but has renal effects. The renal effects differ between systems studied. In the rat, misoprostol reduces cyclosporin-induced renal tubular toxicity, whereas in humans it has been shown to attenuate renal allograft rejection. Sucralfate is the aluminium salt of sucrose octasulfate. It permits the absorption of aluminium in amounts similar to aluminium-containing antacids, and toxicity has been demonstrated in the presence of renal insufficiency. Bismuth compounds are used increasingly to treat peptic ulcer disease, and bismuth toxicity has been described in association with renal insufficiency. Aluminium-, calcium- and magnesium-containing antacids are used as oral phosphate binders in patients with renal insufficiency in addition to their usual indications. Cation absorption and accumulation with all of these antacid preparations has been described and may lead to toxicity.

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“…Divalent cations have been shown to prevent mucosal injury, although the mechanisms responsible are still controversial (Szabo et a1 1981;Esplugues et a1 1985;Dupuy & Szabo 1986). As shown in Table 4, pretreatment with indomethacin prevents the defensive effects of almagate, thus suggesting that the protective effects of the compound are related to an increase in endogenous gastroprotective prostaglandins (Whittle & Esplugues 1989;Walt 1990;Whittle 1993).…”

Section: I1mentioning

confidence: 99%

Protection by Almagate of Ethanol-induced Gastric Mucosal Damage in Rats

Barrachina

Martínez-Cuesta

Calatayud

et al. 1995

Journal of Pharmacy and Pharmacology

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The study was designed to analyse the protective effects of almagate on a model of gastric injury, ethanol-induced mucosal damage, in which acid plays little, if any, role. Pretreatment with almagate dose-dependently reduced the level of gastric damage induced by oral administration of 1 mL 100% ethanol. Administration of 12 mumol kg-1 alamagate 30 min before ethanol significantly reduced the area of mucosal damage by 65 +/- 10%, and the maximum level of inhibition (74 +/- 11%) was obtained with 150 mumol kg-1 almagate. Administration of higher doses of almagate (200-250 mumol kg-1) did not result in any further increase in the level of protection against ethanol-induced gastric damage. Administration of 1 mL 100% ethanol induces substantial damage to the gastric mucosa, with nearly 40% of the length of the section evaluated exhibiting deep necrotic and haemorrhagic damage. Pretreatment with almagate caused a significant diminution in all parameters of histological damage, whereas damage to the epithelial cell layer was only significantly reduced by pretreatment with the highest doses evaluated (25, 50 and 150 mumol kg-1). Administration of aluminium hydroxide did not modify ethanol-induced mucosal damage, even at doses containing concentrations of aluminium higher than those present in gastroprotective doses of almagate. Pretreatment with sucralfate, another aluminium containing compound, at doses of 250 mumol kg-1 protected the mucosa, although lower doses did not. The present study has shown that almagate prevents ethanol-induced gastric mucosal damage.(ABSTRACT TRUNCATED AT 250 WORDS)

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Prostaglandins and Peptic Ulcer Therapy

Cited by 15 publications

References 47 publications

Developmental Changes in Gastric Mucus Gel Thickness: Responsiveness to 16,16-Dimethyl Prostaglandin E2 and Mucosal Protection in the Rat

Developmental Changes in Gastric Mucus Gel Thickness: Responsiveness to 16,16-Dimethyl Prostaglandin E2 and Mucosal Protection in the Rat

Renal Effects of Peptic Ulcer Therapy

Protection by Almagate of Ethanol-induced Gastric Mucosal Damage in Rats

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