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Abstract
The objective of this study was to gather evidence for production of nitric oxide
(NO) during a primary infection with the protozoan parasite Eimeria tenella, which
carries out its life cycle in the ceca of chickens. Relationships of plasma levels
of NO2(-)+NO3-, stable metabolites of NO, with parasite dose and with time after infection
were examined, as well as effects of administration of aminoguanidine, an inhibitor
of induced nitric oxide synthase (iNOS). Inoculation with 5 x 10(4) and 1 x 10(6)
but not 1 x 10(3) oocysts per chick caused significant (P < or = 0.05) increases in
micromolar concentrations of plasma NO3(-)+NO3- when measured at 7 d postinoculation
(PI). In chickens inoculated with 5 x 10(4) oocysts, significant (P < or = 0.05) increases
in plasma NO2(-)+NO3- were seen at 5 and 7 but not 3 d PI. Daily intraperitoneal administration
of 1.25 mg per chick aminoguanidine during the period of infection did not lower the
increases in plasma NO2(-)+NO3- seen at 5 and 7 d PI, and did not affect the degree
of colonization of the cecal tissue by the parasite. However, administration of aminoguanidine
did alter the gross appearance of the ceca, which were less swollen and filled with
blood at 5 and 7 d PI as compared with ceca from untreated chickens. Hemorrhage is
a major pathological manifestation of E. tenella infections, associated with the disruption
of the cecal mucosa by the developing parasite. The results of this experiment are
consistent with the hypothesis that an aminoguanidine-inhibitable NO synthase, perhaps
in the vascular endothelium of the cecal blood vessels, may contribute to hemorrhage
by causing vasodilation.