RESUMO
The purpose of the present study was to evaluate the effect of treatment with oxamniquine on the portal pressure of mice infected with Schistosoma mansoni. The animals were infected with 30 cercariae and portal pressure was measured with a polygraph at 70 (acute phase) and 160 (chronic phase) days after infection. On days 70 and 160 two other groups of infected mice were treated with 400 mg/kg of oxamniquine and portal pressure was measured 90 days later (160 and 250 days after infection). A group of uninfected mice was used as control. The measured portal pressures, in mmHg, were: matched uninfected control mice 8.7+/-2.1 and acute phase group, measured at day 70, 13.4+/-3.5. Matched uninfected control 7.5+/-0.6 and chronic phase group, measured at day 160 post-infection, 11.6+/-1.5. Matched uninfected mice 6.9+/-0.9 and chronic phase group, measured at day 250, 10.4+/-1.8. Oxamniquine-treated at day 70 and measured at day 160 7.9+/-0.4; oxamniquine-treated at day 160 and measured at day 250, 7.6+/-1.7. The infection of mice with 30 cercariae of S. mansoni induced portal hypertension, both during the acute and chronic phases and treatment with oxamniquine caused portal pressure to return to normal levels.
Assuntos
Hipertensão Portal/tratamento farmacológico , Oxamniquine/uso terapêutico , Esquistossomose mansoni/tratamento farmacológico , Esquistossomicidas/uso terapêutico , Animais , Hipertensão Portal/etiologia , Masculino , Camundongos , Esquistossomose mansoni/complicaçõesRESUMO
Outbred male albino mice normal or infected with 30 cercariae of Schistosoma mansoni (LE strain) were submitted to 65% hepatectomy during the acute (70 days) and chronic phase (160 days) phases of the disease. A group of the infected animals was treated with 400 mg/kg of oxamniquine during the acute phase before hepatectomy. Non-infected, infected and treated but not hepatectomized animals were kept as controls. Hepatic regeneration was evaluated by incorporation of tritiated thymidine, intraperitoneally injected into non-hepatectomized and hepatectomized animals, 24 hours after surgery. The results showed that removal of 65% of the hepatic parenchyma, during the acute phase, led to a statistically significant increase of thymidine incorporation, when compared with the uninfected hepatectomized controls. This phenomenon was not observed at the chronic phase. Treatment with oxamniquine administered during the acute phase led to a decrease in thymidine incorporation rate 160 days after infection (90 days after treatment) and 24 hours after hepatectomy. The data suggest that infection with S. mansoni represents a considerable stimulus for the regenerative capacity of the liver during the acute, but not the chronic phase of disease.
Assuntos
Hepatectomia , Regeneração Hepática , Oxamniquine/uso terapêutico , Schistosoma mansoni , Esquistossomose mansoni/tratamento farmacológico , Esquistossomicidas/uso terapêutico , Doença Aguda , Animais , Doença Crônica , Masculino , Camundongos , Esquistossomose mansoni/induzido quimicamente , Timidina/metabolismoRESUMO
Outbred male albino mice normal or infected with 30 cercariae of Schistosoma mansoni (LE strain) were submitted to 65 percent hepatectomy during the acute (70 days) and chronic phase (160 days) phases of the disease. A group of the infected animals was treated with 400 mg/kg of oxamniquine during the acute phase before hepatectomy. Non-infected, infected and treated but not hepatectomized animals were kept as controls. Hepatic regeneration was evaluated by incorporation of tritiated thymidine, intraperitoneally injected into non-hepatectomized and hepatectomized animals, 24 hours after surgery. The results showed that removal of 65 percent of the hepatic parenchyma, during the acute phase, led to a statistically significant increase of thymidine incorporation, when compared with the uninfected hepatectomized controls. This phenomenon was not observed at the chronic phase. Treatment with oxamniquine administered during the acute phase led to a decrease in thymidine incorporation rate 160 days after infection (90 days after treatment) and 24 hours after hepatectomy. The data suggest that infection with S. mansoni represents a considerable stimulus for the regenerative capacity of the liver during the acute, but not the chronic phase of disease