Abstract
To arrive at a basic understanding of the pathogenesis of reflux esophagitis, we developed an acute experimental model in the rabbit for studying the early lesion. Acid was perfused in vivo into the lower esophagus while potential difference was monitored intermittently. At varying degrees of potential difference decline, indicating epithelial injury, the esophageal stratified squamous epithelial tissue was removed for morphologic studies and in vitro electrophysiologic and transport studies. At 50% reduction in potential difference, there was dilation of intercellular spaces, which when correlated with physiologic results of increased permeability indicates increased intercellular water. At 100% reduction in potential difference, cells in the midepithelium were observed to be swollen and ruptured, forming vesicular spaces, midepithelial cleavages, and later early ulceration. Results of functional studies at this stage showed inhibition of sodium transport. The midepithelial site of disruption corresponds to the site of active sodium pumping out of cells in other stratified squamous epithelia. Since sodium is transported by esophageal epithelium and this function was inhibited by acid, we propose that this early morphologic lesion may be the result of damage to the sodium-transporting mechanisms of the epithelium.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 198-208 |
| Number of pages | 11 |
| Journal | Laboratory Investigation |
| Volume | 45 |
| Issue number | 2 |
| State | Published - 1981 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Pathology and Forensic Medicine
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Morphologic alterations in early acid-induced epithelial injury of the rabbit esophagus. / Carney, C. N.; Orlando, R. C.; Powell, D. W.; Dotson, M. M.
In: Laboratory Investigation, Vol. 45, No. 2, 1981, p. 198-208.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Morphologic alterations in early acid-induced epithelial injury of the rabbit esophagus
AU - Carney, C. N.
AU - Orlando, R. C.
AU - Powell, D. W.
AU - Dotson, M. M.
PY - 1981
Y1 - 1981
N2 - To arrive at a basic understanding of the pathogenesis of reflux esophagitis, we developed an acute experimental model in the rabbit for studying the early lesion. Acid was perfused in vivo into the lower esophagus while potential difference was monitored intermittently. At varying degrees of potential difference decline, indicating epithelial injury, the esophageal stratified squamous epithelial tissue was removed for morphologic studies and in vitro electrophysiologic and transport studies. At 50% reduction in potential difference, there was dilation of intercellular spaces, which when correlated with physiologic results of increased permeability indicates increased intercellular water. At 100% reduction in potential difference, cells in the midepithelium were observed to be swollen and ruptured, forming vesicular spaces, midepithelial cleavages, and later early ulceration. Results of functional studies at this stage showed inhibition of sodium transport. The midepithelial site of disruption corresponds to the site of active sodium pumping out of cells in other stratified squamous epithelia. Since sodium is transported by esophageal epithelium and this function was inhibited by acid, we propose that this early morphologic lesion may be the result of damage to the sodium-transporting mechanisms of the epithelium.
AB - To arrive at a basic understanding of the pathogenesis of reflux esophagitis, we developed an acute experimental model in the rabbit for studying the early lesion. Acid was perfused in vivo into the lower esophagus while potential difference was monitored intermittently. At varying degrees of potential difference decline, indicating epithelial injury, the esophageal stratified squamous epithelial tissue was removed for morphologic studies and in vitro electrophysiologic and transport studies. At 50% reduction in potential difference, there was dilation of intercellular spaces, which when correlated with physiologic results of increased permeability indicates increased intercellular water. At 100% reduction in potential difference, cells in the midepithelium were observed to be swollen and ruptured, forming vesicular spaces, midepithelial cleavages, and later early ulceration. Results of functional studies at this stage showed inhibition of sodium transport. The midepithelial site of disruption corresponds to the site of active sodium pumping out of cells in other stratified squamous epithelia. Since sodium is transported by esophageal epithelium and this function was inhibited by acid, we propose that this early morphologic lesion may be the result of damage to the sodium-transporting mechanisms of the epithelium.
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M3 - Article
VL - 45
SP - 198
EP - 208
JO - Laboratory Investigation
JF - Laboratory Investigation
SN - 0023-6837
IS - 2
ER -