title: Contribution of lactate buffer, glucose and glucose degradation products to peritoneal injury in vivo.
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.
authors: Department of Molecular Cell Biology, VU University Medical Center, 1007 MB Amsterdam, The Netherlands.
authors: Mohammad
authors: M
authors: Zareie
authors: Liesbeth H P
authors: LH
authors: Hekking
authors: Angelique G A
authors: AG
authors: Welten
authors: Bas A J
authors: BA
authors: Driesprong
authors: Inge L
authors: IL
authors: Schadee-Eestermans
authors: Dirk
authors: D
authors: Faict
authors: Anne
authors: A
authors: Leyssens
authors: Casper G
authors: CG
authors: Schalkwijk
authors: Robert H J
authors: RH
authors: Beelen
authors: Piet M
authors: PM
authors: ter Wee
authors: Jacob
authors: J
authors: van den Born
mesh_terms: D000818:Animals; D002021:Buffers; D015314:Dialysis Solutions / Q000009:adverse effects*; D005947:Glucose / Q000009:adverse effects*; D017127:Glycation End Products, Advanced; D006863:Hydrogen-Ion Concentration; D019344:Lactic Acid / Q000009:adverse effects*; D008297:Male; D023421:Models, Animal; D009852:Omentum / Q000473:pathology; D010531:Peritoneal Dialysis, Continuous Ambulatory / Q000009:adverse effects* / Q000379:methods; D010532:Peritoneal Diseases / Q000209:etiology / Q000473:pathology*; D010537:Peritoneum / Q000473:pathology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D002021:Buffers; D015314:Dialysis Solutions; D017127:Glycation End Products, Advanced; D019344:Lactic Acid; D005947:Glucose