Nitric oxide is involved in the lesions of the peripheral autonomic neurons observed in the acute phase of experimental Trypanosoma cruzi infection

Our aim was to investigate the possible involvement of nitric oxide (NO) in peripheral denervation during the acute phase of murine experimental Trypa nosoma cruzi infection. Wistar male rats were infected with the Y strain of T. cruzi. One group of animals was also treated with the NO synthase inhib itor N-nitro-L-arginine. A group of uninfected animals was the control. At the 18th day of infection the animals were sacrificed. Quantification of ne urons in the colon and heart and tissue parasitism in the heart was perform ed. Serum concentration of nitrate was measured and a histochemical techniq ue for assessing NADPH-diaphorase activity in the colon was also performed. The infected animals presented a statistically significant decrease in the number of peripheral neurons in the colon and heart and a 2-fold increase in serum NO3 concentration compared with controls. The animals treated with N-nitro-L-arginine showed almost an absence of NO3 concentration in the se rum and did not show loss of neurons compared with controls. These treated animals displayed a 15-fold increase in tissue parasitism compared with non treated infected animals. The NADPH-diaphorase activity was much more inten se in the muscle layers of the colon of the infected animals than in those of the controls. Taken together, these data suggest that NO is involved in the peripheral denervation observed in the acute phase of experimental T. c ruzi infection. (C) 1999 Academic Press.