Trypanosoma cruzi
infection induces diverse alterations in immunocompetent cells and organs, myocarditis
and congestive heart failure. However, the physiological network of disturbances imposed by the infection has not
been addressed thoroughly. Regarding myocarditis induced by the infection, we observed in our previous work that
Fas-L-/- mice (
gld/gld) have very mild inflammatory infiltration when compared to BALB/c mice. However, all mice
from both lineages die in the early acute phase. Therefore, in this work we studied the physiological connection relating
arterial pressure, renal function/damage and cardiac insufficiency as causes of death. Our results show that
a broader set of dysfunctions that could be classified as a cardio/anaemic/renal syndrome is more likely responsible
for cardiac failure and death in both lineages. However,
gld/gld mice had very early glomerular deposition of IgM
and a more intense renal inflammatory response with reduced renal filtration, which is probably responsible for the
premature death in the absence of significant myocarditis in
gld/gld.
