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Fluoride, a well-recognised harmful substance, is easily absorbed by the gastrointestinal mucosa. It is therefore conceivable that any alteration of the gastrointestinal motility can affect the rate of absorption of fluoride and leads to aggravation of its toxic effects. The effects of fluoride on gastric emptying and intestinal transit were studied in the mouse using a carboxymethyl cellulose (CMC) solution as a non-nutrient meal. The participation of the cholinergic and nitrergic systems in these effects was also evaluated. Oral gavage of 5 mM NaF had no significant effect on gastric emptying and intestinal transit of the CMC meal, whereas a decrease of gastric emptying (-33%, P

The gastric cytoprotective properties of natural honey (monofloral and polyfloral specimens) and of a glucose-fructose-sucrose-maltose mixture (GFSM) was evaluated in the rat using absolute ethanol, indomethacin and acidified acetylsalicylic acid (ASA-HCl) as necrotising agents. Prior gastric administration of honey (2.5 g/kg) to animals induced a net reduction of hemorrhagic lesions length of the mucosa. Protection of the stomach elicited by both types of honey and GFSM was almost total against ethanol-induced lesions. Similar results were also observed when using ASA-HCl except that the percent protection was 87%. The percent reduction of indomethacin-induced gastric lesions was variable according to the nature of the test solution: GFSM mixture (41.1%) < polyfloral honey (55.2%) < monofloral honey (64.0%). Perfusion of the stomach with isotonic honey resulted in (1) a 70% reduction of the area of the lesions caused by ethanol, (2) the failure to prevent the transmural potential difference fall induced by ethanol, (3) an increase of basal and histamine-stimulated acid secretion. These results suggest that sugar rich solutions (GFSM and honey) may prevent gastric damage by a mechanism involving the release of some protective agents.

Summary Background: We have previously shown that natural honey is able to protect the rat stomach against acute ethanol- and indomethacin-induced lesions. The present investigations were undertaken to examine the role of intraluminal osmolality in this protective effect. Methods: Mannitol, glucose-fructose-sucrose-maltose mixture (GFSM) and natural honey (300, 600, 1800 mOsmol/kg water) were given orally to rats 30 min before administration of 70% ethanol for a further 15-min period. Lesions area of the excised stomachs were evaluated. Pylorus-ligated stomachs were filled with mannitol, GFSM mixture and honey (1800 mOsmol/kg water) to test the effect of the hyperosmolar solutions on gastric fluid content and acid secretion. The rate of gastric emptying of the three test solutions (1800 mOsmol/kg) was measured by the phenol red method. Results: Intragastric administration of mannitol, GFSM mixture or honey prevented the formation of mucosal lesions in an osmolality-dependent manner. Using the pylorus-ligated stomach model, the test solutions led to a net increase of luminal fluid volume without affecting acid content. Hyperosmolar solutions presented a delayed gastric emptying if compared to a nonnutrient solution made of carboxymethyl cellulose. Conclusions: The observed results suggest that hyperosmolar solutions can prevent the formation of hemorrhagic lesions by luminal dilution of the necrotising agent and acid, an effect which may be potentiated by a lowered gastric emptying rate.