Functional and histological injury to intestinal mucosa produced by hypertonicity

Kubo, Hiroshi; Abei, Toru; Nasrallah, Salah M.; Iber, FL

doi:10.1152/ajplegacy.1968.214.5.1090

Cited by 62 publications

(25 citation statements)

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“…During the osmotic equilibration following the force-feeding there was a significant loss of cells from the jejunum, a loss of brush border disaccharidases into the intestinal lumen and focal ultrastructural damage. These findings are consistent with previous observations (10,14,19,22,23) of osmotic equilibration and intestinal damage in isolated duodenal and ileal loops as well as in intestinal preparations perfused directly with hypertonic solutions.…”

Section: Mucosa: Electron Microscopysupporting

confidence: 93%

“…Thus, in the earlier studies noted above, the most extensive damage was produced when as much as 50% glucose was perfused directly into the gut (14). In the present study, where the hyperosmotic agent was given into the stomach, intestinal damage was much milder (see Refs.…”

Section: Mucosa: Electron Microscopysupporting

confidence: 52%

“…Direct perfusion of hypertonic solutions into the small intestine produces a rapid response, including osmotic equilibration (10,23) and morphologic (14,19,23) and functional damage (9,14,22). Small intestinal hyperosmotic stress, which occurs during diarrheal disease (1, 15) and in feedings of hyperosmotic elemental diets to newborn infants (3), may also lead to pathologic changes in the intestine.…”

Section: Speculationmentioning

confidence: 99%

“…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.Direct perfusion of hypertonic solutions into the small intestine produces a rapid response, including osmotic equilibration (10, 23) and morphologic (14,19,23) and functional damage (9,14,22). Small intestinal hyperosmotic stress, which occurs during diarrheal disease (1, 15) and in feedings of hyperosmotic elemental diets to newborn infants (3), may also lead to pathologic changes in the intestine.…”

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Response of Rat Intestine to a Hyperosmotic Feeding

et al. 1978

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SummaryAfter 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 hypertoilically fed rats there was an accumulation of protein, DNA, I3H]thymidinelabeled 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 forcefeeding. 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. SpeculationThe 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.Direct perfusion of hypertonic solutions into the small intestine produces a rapid response, including osmotic equilibration (10, 23) and morphologic (14,19,23) and functional damage (9,14,22). Small intestinal hyperosmotic stress, which occurs during diarrheal disease (1, 15) and in feedings of hyperosmotic elemental diets to newborn infants (3), may also lead to pathologic changes in the intestine. However, oral feedings of hyperosmotic mannitol did not produce any histologic damage to the intestinal mucosa of normal men (2 1).In the present study we have evaluated the effects of a per oral hyperosmotic load upon the physiology and morphology of the small intestinal mucosa of the rat. Our results suggest that a single feeding of a hyperosmotic solution of mannitol produces significant damage to the jejunum. There is a loss of disaccharidase activity associated with a loss o...

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Section: Mucosa: Electron Microscopysupporting

confidence: 93%

Section: Mucosa: Electron Microscopysupporting

confidence: 52%

Section: Speculationmentioning

confidence: 99%

mentioning

confidence: 99%

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Response of Rat Intestine to a Hyperosmotic Feeding

et al. 1978

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“…KAMEDA et al (1968) showed histologically that an exposure of the intestinal mucosa to a hypertonic solution, e.g., a solution 550 mOsm/liter higher than the isotonic, caused some damage of tissue, such as the necrosis of the epithelial cells or the increased exfoliation of the epithelium at the tip of the villi. LOESCHKE et al (1971) also showed that a prolonged exposure to a solution of a moderate hypertonicity caused the similar histological changes.…”

Section: Discussionmentioning

confidence: 99%

Effects of Mucosal Hyperosmolarity on Active Sugar Transport and the Sugar-Evoked Potential in Isolated Small Intestine of the Toad

Saito

Hoshi

1973

Jpn.J.Physiol

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Summary Isolated small intestines of toads were mounted in a flux chamber or suspended from a cannula as an everted sac, and osmolarity of solutions bathing the mucosal surface was changed by adding Dmannitol or polyethylene glycol to the standard solution. With increase in osmolarity we observed increases in (1) resistance of transmural water flow, (2) transmural electrical resistance, (3) tissue electrolyte content, (4) a decrease in water content of the tissue, (5) a change in transmural potential difference in the direction that the mucosal side becomes more positive, and (6) a reduction in size of the glucose-evoked potential. On the other hand the tissue uptake of D-glucose and Dgalactose from the mucosal solution did not significantly change with the treatment. Within a range of osmolarity change (less than 200 mOsm/ liter), results (3) and (4) can be interpreted as due to a mere withdrawal of water from the tissue. The relationship between the size of the osmotic potential change and the osmolarity difference was similar to that between the rate of net water flow and the osmolarity difference. The fact that mucosal hyperosmolarity exerts strong influence on the sugarevoked potential but no significant influence on the uptake of sugar is interpreted as the effect of the hyperosmolarity being a consequence of changes in electrical resistance representing the lateral intercellular space.An elevation or a reduction of osmolarity of the solution bathing the mucosal surface of the small intestine is known to cause changes in passive permeability to water and organic solutes and in the transmural potential of the tissue. LOES-CHKE et al. (1970 have shown that osmotic water flow permeability and passive permeability to sugar molecules measured in the presence of phlorizin are distinctly higher in the presence of mucosal to serosal water flow than in the presence of water flow in the reverse direction. They ascribed such observed asymmetry to different structural changes which were induced concomitantly by osmotic gradients with different directions. SMYTH and WRIGHT (1966) showed that the transmural potential difference of the small intestine was altered by changing osmolarity of the mucosal solution, and LOESCHKE et al. (1971) showed that the magnitude of such osmotic potential changes were also asymmetrical depending on the direction of elicited water flow. Similar asymmetrical permeability characteristics and the relation of them to structural changes in the epithelial cells induced by osmotic water flow have extensively been studied in the gall bladder (TORME and DIAMOND, 1967;SMULDERS et al., 1972;WRIGHT et al., 1972). The effect of transmural osmotic gradients on the active transport of nonelectrolytes by the small intestine has not been studied extensively. PARSO and WINGATE (1961) found that changes in osmolarity of the mucosal solution by changing sodium concentration had little effect on glucose transport in rat small intestine. However, DINDA et al. (1972) observed in hamster intestine a unique eff...

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On Certain Physical-Chemical Properties of Infant Formulas

Segar¹,

Chesney²

1977

Arch Pediatr Adolesc Med

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Functional and histological injury to intestinal mucosa produced by hypertonicity

Cited by 62 publications

References 0 publications

Response of Rat Intestine to a Hyperosmotic Feeding

Response of Rat Intestine to a Hyperosmotic Feeding

Effects of Mucosal Hyperosmolarity on Active Sugar Transport and the Sugar-Evoked Potential in Isolated Small Intestine of the Toad

On Certain Physical-Chemical Properties of Infant Formulas

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