Abstract: AIM: To study nitric oxide-induced early preconditioning of cardiac myocytes and its signal transduction pathways.METHODS: Cultured neonatal rat cardiac myocytes were pretreated with SNAP and L-Arg respectively for 1 h.The injury of cardiac myocytes was detected after subsequent 6 h hypoxia to determine whether NO could induce early preconditioning.Cells were incubated with cGMP inhibitor methylene blue, protein kinase C (PKC) inhibitor D-sphingosine, calcium antagonist lacidipine and adenosine triphosphate sensitive potassium channel [ K (ATP) channel] blocker libenclamide respectively for half an hour.Cells were then treated with SNAP for 1 h.Cardiac myocytes injury was observed by detecting cell viability and lactate dehydrogenase (LDH).RESULTS: Both SNAP and L-Arg could induce early preconditioning of cardiac myocytes, nitric oxide synthase (NOS) inhibitor L-NAME block the protective effect of L-Arg, Methylene blue could completely abolish SNAPinduced cardioprotection, and D-sphingosine, lacidipine and glibenclamide weaken SNAP-induced protection.CONCLUSION: NO can induce early preconditioning protection of cardiac myocytes via cGMP-dependent pathway.Activation of PKC and opening of calcium channels and K(ATP) channels may be important downstream events of cGMP.

Key words: nitric oxide, cardiac myocyte, hypoxia, preconditioning, signal transduction