Response of Rat Intestine to a Hyperosmotic Feeding

Summary: After a single force-feeding of hypertonic (1300 mOsm) mannitol to rats there is rapid osmotic equilibration of the jejunal fluid, a sharp drop in luminal mannitol concentration and large influxes of water and sodium. During osmotic equilibration there was a significant loss of cells from the jejunal mucosa. In hypertoaically fed rats there was an accumulation of protein, DNA, [3H] thymidine-labeled DNA, and disaccharidases in intestinal washings. Brush border disaccharidase specific activities on the jejunal mucosa were unaltered. Under the light microscope jejunal villi from hypertonic mannitol rats were comparable to controls. Some epithelial cells from rats force-fed hypertonic mannitol showed transient ultrastructural damage. Microvilli of some cells were shortened and fused at their bases 20 and 40 min after the force-feeding. By 120 min epithelial cell microvilli were all normal in appearance. In hypertonically fed rats the lateral interdigitating plasma membranes became disorganized. Large fragments budded off into one cell and fused to form larger structures. By 120 min many lysosomal autophagic vacuoles and residual bodies were seen. A single hypertonic force feeding produced jejunal cell loss associated with loss of brush border disaccharidases and focal ultrastructural damage.Speculation: The damage induced in the jejunal mucosa of rats by a hypertonic feeding may provide clues concerning the pathophysiology of certain clinical conditions. Damage to the lateral interdigitating plasma membranes of adjacent epithelial cells could reflect alterations in permeability allowing the passage of bacterial toxins or allergens into the circulation, or permitting massive bacterial gas leakage leading to pneumatosis intestinalis. The loss of jejunal cells and parallel loss of disaccharidases into the intestinal lumen could, in part, account for the disaccharidase deficiences seen in diarrheal disease where osmotic pressure can become significant because of unabsorbed carbohydrate. This malabsorption may be further enhanced by microvillar alterations such as shortening and fusion, which significantly decrease the effective absorptive area.

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