The brief methylprednisolone administration is crucial to mitigate cardiac dysfunction after myocardial infarction

• Autor(a) principal: Bahr, Alan Christhian
• Data de Publicação: 2021
• Outros Autores: Luz, Julia Paim da, Teixeira, Rayane Brinck, Turck, Patrick, Zimmer, Alexsandra, Castro, Alexandre Luz de, Reis, Eduardo Echer dos, Visioli, Fernanda, Belló-Klein, Adriane, Araújo, Alex Sander da Rosa, Schenkel, Paulo Cavalheiro
• Tipo de documento: Artigo
• Idioma: eng
• Título da fonte: Repositório Institucional da UFRGS
• Texto Completo: http://hdl.handle.net/10183/232629
• topic: Infarto do miocárdio; Acetato de metilprednisolona; Estresse oxidativo; Metaloproteinase 2 da matriz; Acute myocardial infarction; Heart failure; Metalloproteinase; Methylprednisolone acetate

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.