The effects of hyperosmolar agents lithium chloride and sucrose on the brain concentration of diminazene aceturate in rats.

The concentrations of diminazene aceturate in the brain of Trypanosoma brucei brucei infected and uninfected rats treated with diminazene aceturate (3.1 mg/kg, im) and either LiCl (2.5, 5.0 and 10 micrograms/kg) or sucrose (0.25, 0.5 and 1.0 g/kg) were determined. When diminazene aceturate was administered at a standard dose of 3.1 mg/kg (im), the addition of LiCl (10 micrograms/kg, im) increased significantly (P < 0.05) the concentration of the drug in the brains of both trypanosome infected and normal infected rats. The addition of sucrose (1.0 g/kg, im) instead of LiCl failed to give any significant increase in diminazene aceturate levels in the brain. The diminazene aceturate levels were significantly (P < 0.05) higher in the organs (brain, kidney, liver and spleen) of trypanosome infected compared to uninfected rats. The concentration of diminazene aceturate in the organs increased significantly (P < 0.05) with increasing concentrations of LiCl.

The chemotherapeutic efficacy of diminazene aceturate and lithium chloride against relapse infection of Trypanosoma brucei brucei in rats.

The chemotherapeutic efficacy of diminazene aceturate (Berenil) and lithium chloride (LiCl) in relapse infection of trypanosomiasis was investigated in rats experimentally infected with Trypanosoma brucei brucei. The study showed that the combination of diminazene aceturate at (7 mg/kg) and LiCl (10 micrograms/kg) appeared more effective therapeutically than diminazene aceturate, or diminazene aceturate and LiCl and dexamethasone group, as more of the rats in the diminazene aceturate and LiCl treated-group remained aparasitaemic for longer days (60 days). Relapse parasitaemia occurred on days 10 and 12 in diminazene aceturate (7 mg/kg); diminazene aceturate (7 mg/kg) and LiCl (10 micrograms/kg) plus dexamethasone (1 mg/kg) treated group respectively, while relapse parasitaemia did not occur in the diminazene aceturate and LiCl treated group until day 20. Histopathological examination of the brain did not show any signs of inflammatory reaction in the diminazene aceturate and LiCl and dexamethasone treated group. However lesions associated with meningoencephalitis, such as cellular infiltration of mononuclear cells, perivascular cuffings and perivascular congestion and oedema were observed in the diminazene aceturate; diminazene aceturate and LiCl treated groups.