OBJECTIVE To determine in vivo effects of nitric oxide (NO) on blood-brain barrier (BBB) permeability in common carp (Cyprinus carpio L.). ANIMALS 148 carp. PROCEDURES Carp received glyceryl trinitrate (1 mg/kg) as an NO donor or received no treatment (control group). Nitrite and nitrate concentrations in carp sera were determined 0.25, 1, 3, 6, 8, 12, and 24 hours after treatment. In control and treatment groups, BBB permeability was analyzed by assessment of leakage of Evans blue dye into various brain areas at 6, 12, and 24 hours after glyceryl trinitrate treatment. Brain edema was determined by means of the wet-dry weight method and assessed with light microscopy on H&E-stained preparations of tissues obtained 6 and 24 hours after glyceryl trinitrate treatment. RESULTS Treatment with glyceryl trinitrate induced endogenous synthesis of NO, which was upregulated 6 and 8 hours after treatment. Increased NO synthesis was associated with increased permeability of the BBB, which developed 6 hours after treatment with the NO donor. Although the BBB became impermeable again by 12 hours after glycerol trinitrate treatment, brain edema still persisted 24 hours after treatment. CONCLUSIONS AND CLINICAL RELEVANCE In this study, treatment with an NO donor caused reversible opening of the BBB and brain edema in common carp. An intact BBB is important to prevent influx of potentially harmful substances into the brain. This investigation highlighted the possibility of BBB disarrangement caused by NO, a substance found in the CNS of all vertebrates evaluated.

Histopathological changes were studied in Swiss albino mice (N:36)which were challenged with the South Indian local strain of Trypanosoma evansi. Each animal was infected with 5×105 trypanosomes intraperitoneally. The animals were examined daily for development of clinical signs and infection status by wet blood-films made from the tail veins. The infected mice were dull and depressed from two days post-infection (DPI) onwards. Systematic post-mortem examination of the infected mice was performed and pathological changes were recorded. The different tissue samples were collected in 10% formalin and were used to study the histopathological changes. Postmortem examination from 3-4 DPI (the maximum period of observation) revealed splenomegaly, hepatomegaly, marked congestion of lungs, presence of fl uid in peritoneal cavity. Histopathologically, heart muscles showed hyaline degenerative changes and haemorrhages. Liver parenchyma revealed congestion of central vein and sinusoids, binucleated hepatocytes and fatty change of hepatic cells. Thickening of interstitial space with mononuclear infiltration, areas of collapse, areas of emphysema, edema and dilated and congested blood vessels were the histopathological changes noticed in the lungs of the infected mice. In the spleen, giant cells aggregation, hyperplasia, thickening of capsule and trabecule were the changes indicating irreversible degeneration. The affected kidney showed inter-tubular hemorrhages in the cortex, medullary hemorrhages, congested glomerulus, atrophied glomerulus, desquamated tubular epithelium and disruption of renal tubules at some places.