Backgroud: Bupivacaine blocks the sodium channels enhanced by hypokalemia. Bupivacaine also inhibits the transient outward K+ current (Ito). Insulin, in contrast, enhances Ito and induces hypokalemia. The current study was performed to confirm the efficacy of insulin for the treatment of bupivacaine- induced cardiac depression in dogs. METHODS: After dogs were anesthetized with pentobarbital, 0.5% bupivacaine was administered at a rate of 0.5 mg/kg/min until S O2 decreased to 60% or less, which was defined as the point of cardiac depression in this study. The insulin group (n = 9, 16.9 +/- 3.1 kg) received 2 ml/kg of a mixed solution of regular insulin 30 units and 5% D/W 50 ml, followed by a glucose infusion (50 ml 5% dextrose in water) over 15 min. The control group (n = 9, 15.8 +/- 3.4 kg) received 2 ml/kg of 5% D/W 50 ml, followed by a normal saline infusion over 15 min. Mean arterial pressure (MAP), heart rate (HR), pulmonary artery pressure (PAP), central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), SO2, blood gas analysis, serum electrolytes, ECG and the local anesthetic concentraton of the blood were taken. RESULTS: Changes in hemodynamic variables and ECG of the insulin group normalized more rapidly than in the control group. There were no statistical differences in serum Na and Ca2 concentratons between the two groups. The serum K concentration of the insulin group was lower than that of the control group after 5 min of resuscitation. The changes in plasma bupivacaine concentration over time were not significantly different between groups. CONCLUSIONS: Insulin is effective in reversing bupivacaine-induced cardiac depression. This study suggests insulin can be considered an immediate treatment for cardiac depression by bupivacaine.