The mechanism of dextrose-enhanced peritoneal mass transport rates.
The mechanism whereby hypertonic dextrose affects peritoneal transport was investigated in a short-term model of peritoneal dialysis using alert intact rabbits. During control (1.5% dextrose) dialyses osmotic ultrafiltration was 0.28 mg/kg/min, the clearance of potassium was 0.98, urea 0.54, phosphate 0.32, and dextrose (reverse) 0.21 ml/kg/min. With 4.25% dextrose, the ultrafiltration rate increased to 0.73 ml/kg/min (P less than 0.02), but solute transport did not increase despite the added convective flux. The posthypertonic exchanges did not differ from control despite the effect of residual dialysate contaminating this peritoneal lavage. By indicator dilution residual volume averaged 12% of total dialysate volume. Acute volume expansion by intravenous dextrose after desoxycorticosterone acetate (DOCA) pretreatment increased the ultrafiltration coefficient, potassium and urea clearances significantly, and DOCA alone was ineffective. It is suggested that in uremic humans hypertonic dextrose dialysis increases peritoneal mass transport rates because the absorbed dextrose causes extracellular volume expansion that cannot be eliminated promptly. No evidence of a direct effect of dextrose augmenting peritoneal permeability was detected.
D000818:Animals; D001692:Biological Transport; D005260:Female; D005947:Glucose / Q000494:pharmacology*; D005950:Glucose Solution, Hypertonic / Q000494:pharmacology; D006801:Humans; D008954:Models, Biological; D010530:Peritoneal Dialysis; D010537:Peritoneum / Q000378:metabolism; D011817:Rabbits; D014462:Ultrafiltration; D014511:Uremia / Q000628:therapy
D005950:Glucose Solution, Hypertonic; D005947:Glucose