DRD2 and myocardial infarction: Ischemia/reperfusion in the heart increased D2R expression; D2R expression was further increased by conditioning and additional treatment with the D2-like receptor agonist bromocriptine, which improved cardiac function, resulting in a more pronounced reduction in apoptosis, cardiomyocyte damage, and myocardial infarct [82,83,84,85].