Experimental pyelonephritis was induced by intravenous inoculation of Staphylococcus aureus in homozygous Brattleboro diabetes insipidus (Hom Brattleboro DI), heterozygous Brattleboro (Het Brattleboro) and Wistar rats. One group of rats from each strain was implanted with morphine-containing pellet three days before inoculation. Another series of groups received D-aspartic acid (D-ASP) intraperitoneally, starting three days before inoculation throughout the experiments. Owing to the inhibition by morphine or D-ASP of food intake, another control group from each strain was subjected to food restriction. Pyelonephritis development on the tenth day of inoculation was evaluated by the determination of viable bacteria in urine and total kidney tissue, and pathomorphological lesions in kidney. Hom Brattleboro DI rats appeared more resistant. Morphine or D-ASP significantly increased the findings in three strains of rat.

No abstract

A comparative study was performed on haematogenous experimental pyelonephritis by injecting a Staphylococcus aureus suspension i.v. to homozygous and heterozygous Brattleboro and Wistar rats. The numbers of viable bacteria in blood, urine and kidney homogenates and the pathomorphological scores determined on the tenth day of infection were significantly lower in Brattleboro diabetes insipidus rats than in heterozygous Brattleboro and normal Wistar rats. The results suggest that homozygous Brattleboro rats are much more resistant to experimental pyelonephritis.

The changes in the production of antibody against Salmonella typhimurium antigen were investigated in rats by means of the agglutination test after chronic oral administration of the L-asparaginase inhibitors morphine (M) or D-aspartic acid (D-Asp) alone or together with L-aspartic acid (L-Asp) and food restriction, all of which had been started five days before the injections of antigen. The statistical evaluation, carried out after the titers had been defined as -log2 of the highest dilution giving a positive agglutination reaction, showed that M or D-Asp significantly decreased antibody production in comparison with the immunized control or food restricted group. The concomitant administration of L-Asp appeared to significantly antagonize the inhibitory effect of both M and D-Asp. Therefore, the results were considered as further supporting evidence for the fact that the deleterious effect of M on the immune system and its functions might be related to the inhibitory effect of M on L-asparaginase activity.