Acute effects of peritoneal dialysis solutions in the mesenteric microcirculation.

Long-term peritoneal dialysis induces morphological changes that may lead to gradual functional impairment of the peritoneal membrane. These changes are characterized by progressive reduction in solute transport or ultrafiltration failure. The mechanism of the peritoneal response to dialysis fluids has not yet been fully elucidated. We used video-microscopy for in vivo evaluation of microhemodynamics and peritoneal microvascular inflammatory response, after a single intraperitoneal exposure of rats to commercial PD fluids: (1) glucose 1.5 % PD solution; (2) lactate buffered glucose 4.25% PD solution; (3) Icodextrin 7%; (4) bicarbonate buffered glucose 3.86% PD fluid; and 5) Hanks solution. Sham-control groups were not injected. A 5-h exposure of the peritoneal membrane to glucose 1.5% PD solution or to Hanks solution did not induce a significant change in leukocyte rolling and adhesion. In contrast, PD solutions containing glucose 4.25% or Icodextrin 7.5% caused a significant 2-3-fold increase in leukocyte rolling (P < 0.001) and adhesion (P < 0.001) and a significant increase in venular blood flow velocity (P < 0.01) and shear rates (P < 0.05 for glucose 4.25%, and P < 0.01 for Icodextrin). Exposure to glucose 3.86% bicarbonate buffered (Physioneal) solution was associated with the lowest values of leukocyte rolling and adhesion among the PD solutions and with extremely higher venular flow velocities and shear rates. A single exposure to conventional PD solutions with a high concentration of glucose (4.25%) or polyglucose (Icodextrin 7.5%) induces changes consistent with an early peritoneal inflammatory response that may be attenuated by the use of bicarbonate-based fluids.

Peritoneal transport after long-term exposure to Icodextrin in rats.

BACKGROUND: Icodextrin, an effective osmotic substance that has been proposed as an alternative agent for peritoneal dialysis induces ultrafiltration over long dwells. This study examines the peritoneal transport after exposure to Icodextrin in rats. METHODS: Animals were divided in 4 groups and injected daily for 30 days with Icodextrin 7.5 % (n = 14), Glucose 4.25 % (n = 19) or glucose 4.25% plus Icodextrin 7.5 % (n = 13). Rats of the control group (n = 15) were not exposed. A 4-hour permeability study was performed using glucose at days 1, 30 and 60. At days 2, 31 and 61 the same animals were injected with Icodextrin. RESULTS: Slopes of effluent sodium at day 30 were significantly higher (p < 0.001) in the glucose (0.006 +/- 0.016), Icodextrin (0.013 +/- 0.014) and mixed groups (0.012 +/- 0.017) than in the control group (-0.041 +/- 0.021). Urea D/P ratio was not significantly different in the 4 groups. After 30 days, glucose effluent levels were significantly lower (p < 0.001) in the glucose (701 +/- 278 mg/dl), Icodextrin (552 +/- 209 mg/dl) and mixed groups (587 +/- 344 mg/dl) than in control rats (1519 +/- 413 mg/dl). Effluent protein (mg/l) in the mixed group (1,555 +/- 357) was significantly higher (p < 0.001) than control (376 +/- 33), glucose (1,015 +/- 232) and Icodextrin (765 +/- 75) groups at day 30. CONCLUSION: The long-term use of Icodextrin does not affect small molecule transport, but induces changes in the peritoneal protein excretion, especially when Icodextrin and glucose are injected together.