Key result
Trypanosoma cruzi infection induces aortic endothelial cell swelling and exposes subendothelial collagen in rats.
Why the study?
Abnormalities of the coronary microcirculation in acute chagasic myocarditis may cause transient ischemia, but the role of aortic endothelial changes in this process is unclear.
No immediate change to Chagas management; leaves open whether endothelial defects drive human microvascular complications.
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.
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M A Rossi (1997) studied Trypanosoma cruzi infection (Chagas disease). Experimental Trypanosoma cruzi infection vs. Uninfected rats (implied) was evaluated on Structural changes of the endothelial lining of the thoracic and abdominal aorta. Experimental Trypanosoma cruzi infection in rats induced aortic endothelial cell swelling and cytoplasm discontinuity exposing subendothelial collagen.
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