Isolated Langendorff perfused hearts (male, Wistar rats) were treated with 50 μM BRT for 30 min before (Pre) or after (Post) 30 min of zero-flow ischemia. Functional outcomes were monitored, with myocardial damage estimated from creatine kinase efflux, infarct size, and left ventricular lipid/protein oxidation assessed by measuring malondialdehyde and protein carbonyls. Ischemia induced contractile dysfunction and cellular injury, with both BRT treatments improving I–R outcomes.
Final post-ischemic recoveries for left ventricular diastolic/developed pressures were significantly enhanced in treated groups: end-diastolic pressure (Control, 78 ± 14, Pre, 51 ± 15*, Post, 51 ± 13 mm Hg*); left ventricular developed pressure, (LVDP; Control 44 ± 15, Pre, 71 ± 19*, Post, 84 ± 13 mm Hg*). Myocardial injury/infarction (MI) was also significantly reduced with BRT treatment: post-ischemic creatine kinase efflux (Control, 1.24 ± 0.41, Pre, 0.86 ± 0.31*, Post, 0.51 ± 0.29 U/g/mL*; infarct size, Control, 67 ± 17, Pre, 39 ± 15*, Post, 22 ± 11%*). These changes were accompanied by significantly reduced malondialdehyde and protein carbonyl content in Pre and Post treated hearts (*P < 0.05 vs. Control).
These data collectively reveal significant cardioprotection upon BRT treatment, with post-treatment being particularly effective. Significant reductions in infarct size and lipid and protein oxidation indicate a mechanism related to protection from oxidative damage and indicate the potential utility of this molecule as a post-MI treatment.