Abstract
Mitochondrial integrity is essential in the maintenance of energy homeostasis and in preventing activation of cell death. In the heart undergoing adverse hypertrophic remodeling, cardiac cells are chronically submitted to stressful conditions. However, whether an increased vulnerability of mitochondria to these stresses prior to cardiac decompensation contributes to disease progression remains largely unknown. In the present study tolerance to stress was assessed in vitro in mitochondria isolated from hypertrophied but non-decompensated rat hearts 12 wks following induction of an aorto-caval fistula (ACF).
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