Peer-reviewed veterinary case report
Correlating structure with solute and water transport in a chronic model of peritoneal inflammation.
- Journal:
- American journal of physiology. Renal physiology
- Year:
- 2006
- Authors:
- Flessner, Michael F et al.
- Affiliation:
- Nephrology Div. · United States
- Species:
- rodent
Abstract
To study the process of chronic peritoneal inflammation from sterile solutions, we established an animal model to link structural changes with solute and water transport. Filtered solutions containing 4% N-acetylglucosamine (NAG) or 4% glucose (G) were injected intraperitoneally daily in 200- to 300-g rats and compared with controls (C). After 2 mo, each animal underwent transport studies using a chamber affixed to the parietal peritoneum to determine small-solute and protein mass transfer, osmotic filtration, and hydraulic flow. After euthanasia, parietal tissues were sampled for histological analysis, which demonstrated significant differences in peritoneal thickness (microm; C, 42.6 +/- 7.5; G, 80.4 +/- 22.3; NAG, 450 +/- 104; P < 0.05). Staining for VEGF correlated with CD-31 vessel counts (no./mm2: C, 53.1 +/- 16.1; G, 166 +/- 32; NAG, 183 +/- 32; P < 0.05). Tissue analysis showed treatment effects on tissue hyaluronan (micro/g: C, 962 +/- 73; G, 1,169 +/- 69; NAG, 1,428 +/- 69; P < 0.05) and collagen (microg/g: C, 56.9 +/- 12.0; G, 107 +/- 12; NAG, 97.6 +/- 11.4; P < 0.05) but not sulfated glycosaminoglycan. Transport experiments revealed no significant differences in mannitol transfer or osmotic flow. Changes were seen in hydrostatic pressure-driven flux (microl x min(-1) x cm(-2): C, 0.676 +/- 0.133; G, 0.317 +/- 0.124; NAG, 0.284 +/- 0.117; P < 0.05) and albumin transfer (microl x min(-1) x cm(-2): C, 0.331 +/- 0.028; G, 0.286 +/- 0.026; NAG, 0.229 +/- 0.025; P < 0.04). We conclude that alteration of the interstitial matrix correlates with diminished hydraulic conductivity and macromolecular transport.
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Search related cases →Original publication: https://pubmed.ncbi.nlm.nih.gov/16118393/