AimUsing neuronal nitric oxide synthase(nNOS) knockout mice and nNOS inhibitor to investigate the effect of nNOS during myocardial ischemic preconditioning.MethodsMice were divided into wild-type ischemia-reperfusion group (WT IR), wild-type ischemic preconditioning group (WT IP), wild-type L-VNIO treatment group (WT IP+L-VNIO), nNOS-/- mice ischemia-reperfusion group (KO IR), nNOS-/- mice ischemic preconditioning group (KO IP).They were subjected to 30 minutes of ischemia by left descending branch of coronary artery ligation followed 3 hours reperfusion.IP was induced by 3 cycles of 5 minutes ischemia and reperfusion before 30 minutes ischemia.After 3 hours reperfusion, terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining and activities of caspase-8, caspase-9, caspase-3, Bax, Bcl-2 and Fas expression were measured.ResultsIn WT group, compared with IR group, TUNEL positive cells, caspase-8, caspase-9, caspase-3 activities and Bax and Fas protein expression were significantly decreased, Bcl-2 expression was significantly increased (p<0.05).In KO group, compared with IR group, TUNEL positive cells, caspase-8, caspase-9, caspase-3 activities and Bax and Fas protein expression were significantly increased, Bcl-2 expression was significantly decreased (p<0.05).ConclusionnNOS was involved in myocardial ischemic preconditioning by reducing myocardial apoptosis.