title: In vitro effects of bicarbonate and bicarbonate-lactate buffered peritoneal dialysis solutions on mesothelial and neutrophil function.
abstract: The inclusion of bicarbonate in the formulation of peritoneal dialysis solutions may avoid the in vitro impairment of certain cell functions seen with acidic lactate-based fluids. The supranormal physiological levels of HCO3- and PCO2 inherent in such formulations may, however, not be biocompatible. This study compared the in vitro biocompatibility of a pH 5.2 lactate-based formulation with formulations containing either 40 mM lactate at pH 7.4, 38 mM HCO3- at pH 6.8 (PCO2 at approximately 240 mm Hg) or 7.4 (PCO2 at approximately 60 mm Hg), and 25 mM HCO3- plus 15 mM lactate at pH 6.8 (PCO2 at approximately 160 mm Hg) or 7.4 (PCO2 at approximately 40 mm Hg). Significant release of lactate dehydrogenase or decreases in ATP content by human peritoneal mesothelial cells (HPMC) and human peripheral polymorphonuclear leukocytes (PMN) after a 30-min exposure to each test solution was only seen with the pH 5.2 lactate-based fluid. The ATP content of HPMC exposed to this fluid returned to control levels after 30 min of recovery in M199 control medium but showed a trend toward decreasing ATP content at 240 min. Similarly, interleukin (IL)-1 beta-induced IL-6 synthesis by HPMC was also only significantly reduced by the pH 5.2 lactate solution. PMN chemiluminescence was unaffected by 30-min exposure to all test solutions except for the pH 5.2 lactate formulation. Staphylococcus epidermidis phagocytosis was reduced to between 46 to 57% of control with all test solutions except the pH 5.2 lactate solution, which further suppressed the chemiluminescence response to 17% of control. These data suggest that short exposure to supranormal physiological levels of HCO3- and PCO2 does not impair HPMC or PMN viability and function. Furthermore, neutral pH lactate-containing solutions show equivalent biocompatibility to bicarbonate-based ones.
authors.affiliation: Institute of Nephrology, University of Wales College of Medicine, Cardiff, United Kingdom.
authors.forename: N
authors.initials: N
authors.lastname: Topley
authors.forename: D
authors.initials: D
authors.lastname: Kaur
authors.forename: M M
authors.initials: MM
authors.lastname: Petersen
authors.forename: A
authors.initials: A
authors.lastname: Jörres
authors.forename: J D
authors.initials: JD
authors.lastname: Williams
authors.forename: D
authors.initials: D
authors.lastname: Faict
authors.forename: C J
authors.initials: CJ
authors.lastname: Holmes
mesh_terms: D000255:Adenosine Triphosphate / Q000378:metabolism; D001639:Bicarbonates / Q000494:pharmacology*; D002021:Buffers; D002470:Cell Survival / Q000187:drug effects; D015314:Dialysis Solutions / Q000494:pharmacology*; D004847:Epithelial Cells; D004848:Epithelium / Q000187:drug effects / Q000502:physiology; D006801:Humans; D015850:Interleukin-6 / Q000096:biosynthesis; D007773:Lactates / Q000494:pharmacology*; D019344:Lactic Acid; D008163:Luminescent Measurements; D009504:Neutrophils / Q000187:drug effects* / Q000502:physiology; D010529:Peritoneal Cavity / Q000166:cytology*; D010530:Peritoneal Dialysis; D010587:Phagocytosis / Q000187:drug effects
chemical_list: D001639:Bicarbonates; D002021:Buffers; D015314:Dialysis Solutions; D015850:Interleukin-6; D007773:Lactates; D019344:Lactic Acid; D000255:Adenosine Triphosphate