Although smaller molecules of dextran (below app. 35 kDa) can normally be eliminated renally, provided urine production is adequate, one important advantage of dextrans relative to other colloids e.g. HES is that dextran can also be fully degraded by dextranase in the liver or reticuloendothelial system to water (H2O) plus carbon dioxide (CO2) which of course means that complete elimination can be achieved via the lungs even in patients with renal insufficiency.
Most of the original research on dextran metabolism using C14 isotope labelling was done some 50-60 years (1, 2) ago when dextrans were first launched as plasma substitutes. An updated study however was performed by Dubick M A et al in 1992 (3) in which he gave isotope (C14) labelled dextran to both normovolemic and hemorrhaged hypovolemic rabbits. After 96 hours, the concentration of C14 -labeled dextran was about 20-fold higher in the liver than in other organs tested (lung, kidney, spleen). Dextranase activity was also significant higher in the liver than in other organs.
As mentioned above, initially (first 2-4 hours) most dextran is excreted renally into the urine - smaller molecules below the renal threshold (Mw 35 -55 kDa) pass through the kidneys leaving larger molecules in circulation. It is then these remaining larger molecules which are metabolized in the liver and reticuloendothelial system to H2O and carbon dioxide CO2.
1. Terry R et. al., Metabolism of dextran - a plasma volume expander. J Lab Clin Med ,42: 6-15, 1953.
2. Ammon R, The presence of dextranase in human tissues. Enzymologia 25, 245-251, 1963.
3. Dubick M, et. al. Dextran metabolism following infusion of 7.5% NaCl / 6% dextran 70 to euvolumic and hemorrhaged rabbits. Drug Develop. Res. 25: 29-38. 1992.
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