Resumo (PT):
Introduction: Cardiac overload is considered an important stimulus for triggering the inital
steps to HF. We hypothesized that exercise training (ExT) could positively influence the
early cardiac adaptation to overload by preserving myocardial integrity and modulating
the triggers of pathways associated with pathological cardiac remodeling.
Material and Methods: Male Wistar rats were randomly divided in 3 groups: Exercise
Overload (Ex+Ov; n=5; 14 week-ExT and acute pressure overload at the end of the study),
Control (CT; n=5; no exercise and no overload) and Control Overload (CT+Ov; n=5; overload
in non exercised animals). At the end of the ExT protocol, animals were prepared for
hemodynamic instrumentation with tip micromanometer pressure catheters. An acute
pressure overload (APO) was induced by constricting the descending aorta (60% LVPmax
elevation) for 120 min. Samples from cardiac tissue were prepared for Light (LM) and
Transmission Electron Microscopy (TEM) and immunohistochemistry (cleaved caspase-3
and Nf-kB).
Results: In comparison with CT group, CT+Ov animals presented intracellular edema and
mitochondrial swelling in both ventricles. Regarding hemodynamic function, alterations
were limited to LV, which showed diastolic dysfunction. Conversely, in Ex+Ov group, APO
resulted in mild signs of cardiac interstitial edema in both ventricles, with no detectable
LV or RV dysfunction. Cleaved caspase-3 and Nf-KB was significantly expressed only in cardiomyocytes
from LV of CT+Ov group. There was no significant expression of caspase-3 or
Nf-kB in cardiomyocytes from RV of both groups.
Conclusion: The present study shows that apoptosis and Nf-kB pathways are activated as
early as 2 hours after LV APO and that ExT seems to be effective in reducing their activation.
We demonstrated that contrarily to sedentary animals, ExT provided functional and
ultra-structural protection in both ventricles. These findings suggest that exercise training
has an important protective role in the modulation of the early cardiac response to pressure
overload.
Language:
Portuguese
Type (Professor's evaluation):
Scientific
Notes:
XXXI Congresso Português de Cardiologia, publicado na Rev. Port. Cardiol. 2010; Vol.29(Sup.I):I-92.