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Acute and long-term changes observed in imprints of mouse mesothelium exposed to glucose-enriched, lactated, buffered dialysis solutions.
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- Additional Information
- Source:
Publisher: Karger Country of Publication: Switzerland NLM ID: 0331777 Publication Model: Print Cited Medium: Print ISSN: 1660-8151 (Print) Linking ISSN: 16608151 NLM ISO Abbreviation: Nephron Subsets: MEDLINE
- Publication Information:
Original Publication: Basel ; New York : Karger
- Subject Terms:
- Abstract:
Solutions for peritoneal dialysis (PD), the hyperosmolarity of which is obtained with glucose, have been shown to initiate and maintain a situation of continuous mesothelial cell injury associated with a process of regeneration which also takes place continuously. The present study was done using the in vivo and almost in situ technique of mesothelial cell imprints. Acute exposure to 4.25% glucose solution at pH 5.2 and 7.0 induced higher mitotic activity, defective cytokinesis, and reduced cell viability. Long-term exposure (15 and 30 days) to both 4.25% glucose solutions was associated with a reduced population density, increased surface area, and lower mesothelial cell viability, regardless of the pH. The use of 1.5% glucose fluid showed that this effect was dose related. After 30 days of recovery, mesothelial cells exposed to the high-glucose solution at both pH 5.2 and 7.0 appeared repopulated by small cells and showed evidence of defective cytokinesis. So far, it appears that the alterations observed after long-term exposure of the mesothelium to PD fluid are mainly caused by the high concentration of glucose per se. The additional effects of hyperosmolarity are still unclear, whereas the eventual role of low pH, at least in the experimental model used here, can be defined as less than marginal.
- Accession Number:
0 (Buffers)
0 (Dialysis Solutions)
0 (Lactates)
IY9XDZ35W2 (Glucose)
- Publication Date:
Date Created: 19950101 Date Completed: 19951124 Latest Revision: 20180215
- Publication Date:
20221213
- Accession Number:
10.1159/000188647
- Accession Number:
7477654
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