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Immune-induced inflammation plays an important role both in aggravating and healing of post myocardial infarction (MI) injuries. Potent anti-inflammatory and local immunomodulatory activity of infliximab has been suggested to have modulating effects on immune responses after MI. The aim of the present study was to evaluate the efficacy of infliximab on hemodynamic responses and myocardial injuries following isoproterenol-induced myocardial infarction. Male Wistar rats, weighting 260 ± 20 g were assigned into ten groups (n = 6) of saline (normal saline), infliximab (7 mg/kg), isoproterenol (100 mg/kg for two consecutive days), and isoproterenol plus infliximab (30 min after the second injection of isoproterenol). The heart tissues and serums were analyzed 24, 48, 72, and 96 h post-MI and hemodynamic parameters, histopathological changes, malondialdehyde (MDA), Total antioxidant capacity (TAC), lactate dehydrogenase (LDH), and lactate levels were assessed in the respective groups. Infliximab partially improved hemodynamic depression in the first days after MI, but the heart became more suppressed later. A similar result also obtained at the MDA tissue levels but not serum levels. Anti-inflammatory effects of Infliximab may improve cardiac function and prevent heart tissue injury early after MI; however, it can worsen the condition later by inhibiting compensatory reactions such as cardiac remodeling and tissue repair. [Display omitted] • Heart tissue remodeling and restoration appear to be prohibited by TNFα inhibition. • Infliximab can block the functions of compensatory mechanisms after myocardial infarction. • Infliximab by interfering in cardiac remodeling can prevent tissue repair in MI. • The dose and timing of immunosuppressive interventions are determinative in MI injuries. [ABSTRACT FROM AUTHOR]