Contribution of lactate buffer, glucose and glucose degradation products to peritoneal injury in vivo
Open Access
- 6 November 2003
- journal article
- research article
- Published by Oxford University Press (OUP) in Nephrology Dialysis Transplantation
- Vol. 18 (12), 2629-2637
- https://doi.org/10.1093/ndt/gfg356
Abstract
Background. Long-term peritoneal dialysis (PD) is associated with the development of functional and structural alterations of the peritoneal membrane. In this study, we investigated the contribution of low pH lactate buffer, high glucose concentration and glucose degradation products to peritoneal injury in a rat peritoneal exposure model. Methods. Rats received daily 10 ml of either heat-sterilized (3.86% glucose, pH 5.2, n = 8) or filter-sterilized PD fluid (3.86% glucose, pH 5.2, n = 8), or lactate buffer (pH 5.2, n = 8) via a mini vascular access port during a 10 week period. Untreated rats served as controls. Results. The low pH lactate buffer instillation induced pronounced morphological changes including the induction of angiogenesis in various peritoneal tissues and mild damage to the mesothelial cell layer covering the peritoneum. It also evoked a cellular response characterized by an increased mesothelial cell density on the liver, the induction of milky spots and accumulation of omental mast cells in the omentum, and significant changes in the composition of peritoneal leukocytes. The addition of glucose to low pH lactate buffer (filter-sterilized PD fluid) strengthened most, but not all of the responses described above and induced a fibrogenic response. In addition to glucose and low pH lactate buffer, the presence of glucose degradation products (heat-sterilized PD fluid) significantly induced an additional omental milky spot response (P < 0.03) and caused profound mesothelial damage. The vessel density in the omentum and the mesentery was significantly correlated to both the number of tissue mast cells and the hyaluronan content in the peritoneal lavage, which might suggest a role for mast cells and hyaluronan in the induction of angiogenesis. Conclusions. Instillations of low pH lactate buffer, a high glucose concentration and glucose degradation products contribute differently and often cumulatively to peritoneal injury in vivo.Keywords
This publication has 9 references indexed in Scilit:
- Inhibition of Prostate Tumor Cell Hyaluronan Synthesis Impairs Subcutaneous Growth and Vascularization in Immunocompromised MiceThe American Journal of Pathology, 2002
- 3,4-Dideoxyglucosone-3-ene (3,4-DGE): A cytotoxic glucose degradation product in fluids for peritoneal dialysisKidney International, 2002
- Hemodynamic Effects of Peritoneal Dialysis Solutions on the Rat Peritoneal MembraneJournal of the American Society of Nephrology, 2002
- Advanced glycation and lipidoxidation of the peritoneal membrane: Respective roles of serum and peritoneal fluid reactive carbonyl compoundsKidney International, 2000
- Dialysis solution containing hyaluronan: Effect on peritoneal permeability and inflammation in ratsKidney International, 2000
- The peritoneal membrane in chronic peritoneal dialysisKidney International, 1999
- Biocompatibility and buffers: Effect of bicarbonate-buffered peritoneal dialysis fluids on peritoneal cell functionKidney International, 1998
- Post-capillary venules in the “milky spots” of the greater omentum are the major site of plasma protein and leukocyte extravasation in rodent models of peritonitisInflammation Research, 1995
- An Elisa Plate Based Assay for Hyaluronan Using Biotinylated Proteoglycan G1 Domain (HA-Binding Region)Matrix, 1990