1  of perfusates with 1 mM mesna or 250 microM dimesna.

2 estigate the hepatic metabolism of mesna and dimesna.

3 th protein-free buffered solution containing dimesna at concentrations observed during therapy.

4                         Extrapolation of the dimesna clearance data from the perfusion model to human

5 egression (r = 0.98; n = 36) to the perfused dimesna concentration (4.2-249 microM), indicating a cle

6 ns, each liver was perfused with up to three dimesna concentrations during consecutive 20-min periods

7                                    Mesna and dimesna concentrations were measured by specific chromat

8                        Mesna was oxidized to dimesna during oxygenation of the perfusate in the reser

9 atched the summed concentration of mesna and dimesna emerging in the effluent perfusate (single-pass

10            The urinary profiles of mesna and dimesna excretion were determined on days 1, 2, and 5; p

11    Our detection of a high ratio of mesna to dimesna in the plasma of clinical samples led us to rein

12 esna is rapidly and irreversibly oxidized to dimesna in the plasma, passes unchanged through the live

13 dy single supratherapeutic concentrations of dimesna or mesna.

14 fusion model to humans suggests that hepatic dimesna reduction may counterbalance the rapid oxidation

15                These data suggested that the dimesna reduction rate was limited by hepatic uptake.

16                                              Dimesna reduction was decreased by agents that deplete g

17                                              Dimesna reduction, adjusted by the effluent flow rate an

18  100 mg/kg ifosfamide did not impair hepatic dimesna reduction.

19                         The concentration of dimesna that entered the liver closely matched the summe

20                      In control experiments, dimesna was not reduced during recirculation through the