Abstract
Mice inoculated three times at intervals of 15 days with epimastigote forms of an 'avirulent' strain of Trypanosoma cruzi and challenged 30 days after the last inoculation with trypomastigote forms of the 'Colombia' strain of T. cruzi develop a cardiomyopathy very similar to that observed in the chronic phase of Chagas' disease in man. The most conspicuous histopathological finding in both human and experimental chagasic cardiomyopathy is focal myocardial necrosis and degeneration. Based on the nature of cell necrosis and degeneration, and the association of this lesion with intravascular platelet aggregation in the experimental model, we suggested that the microcirculation could be involved, via transient ischaemia, in the pathogenesis of chagasic cardiomyopathy. Additional support to this hypothesis is given by the results of the present study showing histochemical evidence of hypoxic changes in the myocardium of mice chronically infected with T. cruzi.
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