Abstract
Acute myocardial infarction (AMI) is one of the major causes of heart failure and mortality. Glucocorticoids administration post-infarction has long been proposed, but it has shown conflicting results so far. This controversy may be associated with the glucocorticoid type and the period when it is administered. To elucidate these, the present aims to evaluate if the brief methylprednisolone acetate administration is determinant for heart adaptation after AMI. Male Wistar rats were divided into 3 groups: sham-operated (SHAM); infarcted (AMI); infarcted treated with methylprednisolone acetate (AMI+M). Immediately after surgery, the AMI+M group received a single dose of methylprednisolone acetate (40 mg/kg i.m.). After 56 days, the cardiac function was assessed and lungs, liver and heart were collected to determine rates of hypertrophy and congestion. Heart was used for oxidative stress and metalloproteinase activity analyses. Methylprednisolone acetate attenuated matrix metalloproteinase-2 activity, cardiac dilatation, and prevented the onset of pulmonary congestion, as well as avoided cardiac hypertrophy. Our data indicate that administration of methylprednisolone acetate shortly after AMI may be a therapeutic alternative for attenuation of detrimental ventricular remodeling.
Highlights
Acute myocardial infarction (AMI) is one of the major health problems worldwide (Phatharajaree et al 2007, Lei & Bin 2019)
In the evaluated therapeutic time window, the treatment was effective in mitigating post-AMI heart dysfunction mainly by the attenuation of left ventricle dilatation and LVEDP
The pharmacological treatment prevented the development of cardiac hypertrophy and pulmonary congestion, which highlights its
Summary
Acute myocardial infarction (AMI) is one of the major health problems worldwide (Phatharajaree et al 2007, Lei & Bin 2019). An early cardiac dysfunction due to the loss of cardiomyocytes post-AMI may lead to heart failure (HF) development over time (Pfeffer & Braunwald, 1990, Teixeira et al 2017). Several mechanisms are related to HF development, such as the increased formation of reactive oxygen species (ROS), the ventricular chambers dilatation, and cardiac fibrosis (Cahill & Kharbanda 2017, Mosterd et al 2001). In this context, oxidative stress and matrix metalloproteinase 2 (MMP-2) play an important role in the HF development (Schenkel et al 2010, Westman et al 2016). Previous studies highlighted the first week after the AMI as critical and decisive in this process, since redoxsensitive signaling pathways are modulated in this time window
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