Abstract: AIM To investigate the role of cardiac deacetylase SIRT3 in cardiopulmonary bypass-induced cardiac dysfunction. METHODSThirty adult Sprague Dawley (SD) rats, aged 4-6 months and weighing 320-420 g, were randomly divided into three groups (n=10 each): sham operation group (sham group, n=10), cardiopulmonary bypass group (CPB group, n=10) and NAD+plus cardiopulmonary bypass group (NAD+treatment group, n=10). CPB model was established by cannulation between right jugular vein and tail arteries. NAD+was given by intraperitoneal injection (2 mg/kg) before CPB. Cardiac function indexes including left ventricular internal diastolic diameter (LVIDd), left ventricular internal diameter at end-systole (LVIDs), fraction shortening (FS) and left ventricular ejection fraction (LVEF) were measured by ultrasound imaging system 1 h after anesthesia resuscitation. SD rats were sacrificed to obtain myocardial specimens. Activity of SIRT3 and AMPK and levels of p-AMPK, AMPK and Glut-4 were measured and analyzed. RESULTSCompared with those in sham group, blood glucose level increased, LVIDd and LVIDs scores in CPB group were significantly higher, FS and LVEF scores were markedly lower, and levels of p-AMPK and Glut-4 and activity of SIRT3 and AMPK decreased (both P<0.05). NAD+treatment significantly decreased blood glucose, increased SIRT3 activity, AMPK activity, levels of p-AMPK, Glut-4, and consequently suppressed CPB-induced impairments of cardiac functions (both P<0.05). CONCLUSIONImpairment of SIRT3 activity with subsequent Glut-4 transfer descent plays an important role in decreased cardiac functions after CPB.