Abstract

In the acute phase of Chagas' disease, the micropathology of the heart reveals a diffuse focal myocarditis, sometimes of a phlegmonous type and of an intensity not seen in any other inflammatory heart disease. Foci of myocytolytic necrosis and degeneration are seen microscopically with an intense mononuclear infiltrate associated with exudative phenomena and marked parasitism of myofibers. Abnormalities of the coronary microcirculation have been demonstrated in acute chagasic myocarditis as possible cause of transient ischemia consistent with the hypothesis of microvascular factor as a cause of the myocardial changes. Considering that the endothelium plays a key role as controller of the vessel tone regulation and vascular permeability, this investigation was carried out to study the structure of the endothelial lining of the thoracic and abdominal aorta obtained from Trypanosoma cruzi-infected rats in the acute septicemic phase by using scanning and transmission electron microscopy. The findings clearly demonstrate that the infected rats developed changes of the endothelial layer characterized by endothelial cell swelling and a few points of cell cytoplasm discontinuity appearing as holes exposing the subendothelial collagen usually associated with platelet-fibrin aggregates. These changes could disturb the generation of vasoactive substances, impairing the equilibrium between opposing forces. The exposition of the subendothelial collagen due to holes in the endothelial lining would favor platelet-fibrin aggregation. This way, the present results allow speculation that similar endothelial cells changes could be present in the microcirculation, reflecting a reduction in the protective role of the endothelium, participating in the genesis of vasospasm and platelet aggregation within coronary microvessels, and leading to the focal pathology in acute chagasic myocarditis.