Is Ethanol‐Induced Damage of the Gastric Mucosa a Hyperosmotic Effect? Comparative Studies on the Effects of Ethanol, some other Hyperosmotic Solutions and Acetylsalicylic Acid on Rat Gastric Mucosa

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Abstract
The involvement of hyperosmolarity in ethanol-induced gastric mucosal damage was studied by comparing the effects of ethanol on the rat gastric mucosa with those caused by hyperosmotic glucose and choline chloride solutions, and by an almost isosmotic solution of acetylsalicylic acid. Upon intragastric instillation, all test solutions, i.e., 3 M and 5 M ethanol (3330 and 5590 milliosmoles/kg, respectively), 3 M glucose (3890 milliosmoles/kg),1.5 M choline chloride (2840 milliosmoles/kg) and 20 mM acetylsalicylic acid, also containing 100 mM HCl and 50 mM NaCl, produced macroscopic and microscopic lesions of the gastric mucosa. The hemorrhages induced by ethanol and acetylsalicylic acid solutions were more evenly distributed, whereas most lesions produced by the glucose and choline chloride solutions were located at the rumeno-fundic junction. There were no qualitative differences between the microscopic lesions caused by the various instillates. All the test solutions broke the gastric mucosal barrier and increased histamine release and pepsinogen output, but in the rats treated with acetylsalicylic acid these effects were less pronounced. Ethanol, glucose and choline chloride solutions increased gastric mucosal flow and fluid output from the stomach, whereas acetylsalicylic acid had no effect on these. The similarity between the ethanol-induced changes and those caused by hyperosmotic solutions of glucose and choline chloride indicates that ethanol may cause damage in the gastric mucosa via hyperosmolarity.

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