The brief methylprednisolone administration is crucial to mitigate cardiac dysfunction after myocardial infarction
| Autor: | ALAN CHRISTHIAN BAHR, JULIA PAIM DA LUZ, RAYANE BRINCK TEIXEIRA, PATRICK TÜRCK, ALEXSANDRA ZIMMER, ALEXANDRE LUZ DE CASTRO, EDUARDO ECHER DOS REIS, FERNANDA VISIOLI, ADRIANE BELLÓ-KLEIN, ALEX SANDER DA ROSA ARAUJO, PAULO CAVALHEIRO SCHENKEL |
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| Jazyk: | angličtina |
| Rok vydání: | 2021 |
| Předmět: | |
| Zdroj: | Anais da Academia Brasileira de Ciências, Vol 93, Iss suppl 4 (2021) |
| Druh dokumentu: | article |
| ISSN: | 1678-2690 0001-3765 |
| DOI: | 10.1590/0001-3765202120210297 |
| Popis: | 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. |
| Databáze: | Directory of Open Access Journals |
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