Persistent activation of 5′-adenosine monophosphate protein-activated kinase signaling, despite the removal of bupivacaine. (A) Western blots of cardiac lysates at different time points during recovery from toxicity with adjuvant IV lipid emulsion (ILE) for acetyl-CoA carboxylase (ACC) phosphorylated at S79, 5′-adenosine monophosphate–activated protein kinase (AMPK) phosphorylated at T172, total AMPK, and total glyceraldehyde-3-phosphate dehydrogenase (GAPDH) as loading control. (B) Western blots of tuberous sclerosis 2 (TSC2) phosphorylated at S1387 and total GAPDH as loading control from cardiac lysates at different time points during recovery from toxicity with bupivacaine (condition = B) and with bupivacaine and adjuvant ILE (condition = BL). (C) Densitometry of phosphoproteins from cardiac lysates comparing relative phosphorylation level of baseline with samples treated with bupivacaine and adjuvant ILE (bupi + ILE; n = 7 for pAMPK and pACC, n = 9 for pTSC2); **P < 0.01, Sidak post hoc test.