As we expected, PRAZ administered intraperitoneally just before BRL treatment significantly abrogated the suppressive effects of BRL on myocardial TNF-α production, caspase-3, p38, JNK and IκBα activation as well as cTnI phosphorylation in septic rats, whereas PRAZ administration did not affect these parameters in septic rats, suggesting that BRL therapy promotes cardiac NE release and suppresses myocardial inflammatory cytokine production and apoptosis thereby reducing myocardial dysfunction in sepsis via NE-induced α1-AR activation. This evidence concerns the gene TNNI3 and Sepsis.