Insights from the use of erythropoietin in experimental Chagas disease.

In addition to the long-established role in erythropoiesis, erythropoietin (Epo) has protective functions in a variety of tissues, including the heart. This is the most affected organ in chronic Chagas disease, caused by the protozoan Trypanosoma cruzi. Despite seven million people being infected with T. cruzi worldwide, there is no effective treatment preventing the disease progression to the chronic phase when the pathological involvement of the heart is often observed. Chronic chagasic cardiomyopathy has a wide variety of manifestations, like left ventricular systolic dysfunction, dilated cardiomyopathy, and heart failure. Since Epo may help maintain cardiac function by reducing myocardial necrosis, inflammation, and fibrosis, this study aimed to evaluate whether the Epo has positive effects on experimental Chagas disease. For that, we assessed the earlier (acute phase) and also the later (chronic phase) use of Epo in infected C57BL/6 mice. Blood cell count, biochemical parameters, parasitic load, and echocardiography data were evaluated. In addition, histopathological analysis was carried out. Our data showed that Epo had no trypanocide effect nor did it modify the production of anti-T. cruzi antibodies. Epo-treated groups exhibited parasitic burden much lower in the heart compared to blood. No pattern of hematological changes was observed combining infection with treatment with Epo. Chronic Epo administration reduced CK-MB serum activity from d0 to d180, irrespectively of T. cruzi infection. Likewise, echocardiography and histological results indicate that Epo treatment is more effective in the chronic phase of experimental Chagas disease. Since treatment is one of the greatest challenges of Chagas disease, alternative therapies should be investigated, including Epo combined with benznidazole.

Effects of acute normovolemic anemia on hemodynamic parameters and Acid-base balance in dogs.

The aim of this study was to evaluate the hemodynamic and acid-base status of dogs subjected to acute normovolemic anemia. The dogs (n = 10) were evaluated 15 minutes and 24 hours after induction of anemia (hematocrit below 18%) with blood withdrawal and simultaneously replacement of same volume of Ringer's lactate solution and hydroxyethyl starch-based solution in a 2 : 1 ratio. The cardiac output was measured by Doppler echocardiography and blood pressure by oscillometric device, and posteriorly hemodynamic parameters were calculated. The anemic groups had increase in cardiac index (P < .05) (3.82 ± 1.05 to 5.86 ± 1.49 and 5.81 ± 1.63 L/min × m(2)) and decreases (P < .05) in the indices of total peripheral resistance (6797.81 ± 3060.22 to 3220.14 ± 1275.02 and 3887.74 ± 1394.89 dina·seg/cm(5) × m(2)) and oxygen delivery (7942.84 ± 3344.00 to 4021.68 ± 1627.00 and 4430.82 ± 1402.61 mL/min × m(2)), respectively. There were no significant changes in pH, but PaO(2) and SaO(2) values were increased, and PaCO(2) reduced in anemic dogs (P < .05). Therefore, acute normovolemic anemia can create significant hemodynamic changes and despite some hemogasometric changes, there were no changes in the acid-base status in dogs.