Affiliations: Cátedra Fisiología Humana, Departamento de Ciencias Fisiológicas, Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Santa Fe 3100, 2000 Rosario, Argentina | Instituto de Inmunología, Departamento de Ciencias Fisiológicas, Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Santa Fe 3100, 2000 Rosario, Argentina | Cátedra de Física Biológica, Departamento de Ciencias Fisiológicas, Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Santa Fe 3100, 2000 Rosario, Argentina
Note: [] Corresponding author: Dr. Alejandra Luquita, Cátedra de Física Biológica, Facultad de Ciencias Médicas, Universidad Nacional de Rosario, Santa Fe 3100, 2000 Rosario, Argentina. Fax: +54 341 448 4761; E‐mail: luquitale@hotmail.com.
Abstract: Microcirculatory alterations would explain focal lesions found in Chagas' cardiomyopathy. Trypanosoma cruzi (T. cruzi) infection induces host blood properties modifications and defensive responses capable of producing blood hyperviscosity, an ischemic risk factor able to affect microvascular blood flow. We studied whole blood viscosity (ηb) and plasmatic and cellular factors influencing it in rats, 7 and 14 days after experimental infection with T. cruzi. Increased plasma viscosity (ηp) was found in infected versus control rats and it was correlated with high blood parasite levels at 7 days and enhanced γ‐globulin fraction concentration at 14 days. The hematocrit, mean corpuscular volume (MCV) and ηb were higher in 14 days infected rats vs. 7 days and control animals. Also, electron microscopy observation showed morphological changes in red blood cells (RBC) at 7 and 14 days post‐infection, with increased proportion of echinocyte and stomatocyte shapes transformation. In our rat model of Chagas' disease, BPL, increased plasmatic protein concentration, enhanced MCV and RBC shapes transformation would determine blood hyperviscosity, cause of microvascular blood flow abnormalities.
