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Background To date,there have been no repots on altered nitric oxide(NO)content in ischemia/reperfusion with regard to in vivo preconditioning procedures.These studies are important for understanding the mechanisms of NO during early myocardialischemic preconditioning.The aim of the present study was to investigate the mechanisms of NO during early myocardial ischemic preconditioning by measuring levels of NO and cyclic guanosine monophosphate (cGMP),as well as activity of nitric oxide synthase(NOS)in ischemia/repedusion with respect to preconditioning in rats.Methods Sixty-six female Sprague-Dawley rats were randomly divided into four groups:ischemic preconditioning group (IP),ischemia/repeffusion group(I/R),control group(CON),and preconditioning procedure group(PC).In the PC group,rats were further divided into PC1-i PC1+,PC2-,PC2+,PC3-,and PC3+ subgroups.Rats unde rwent left coronary artsry occlusion and repeffusion,and subsequently,NOS activity and levels were assessed with spectrophotometric analysis.cGMP contents were measured with radioimmunoassay.Results The level of NO and cGMP,as well as the activity of NOS,were significantly higher in the IP group compared to the I/R and CON groups(P＜0.05).During preconditioning prior to prolonged ischemia,NO and cGMP levels varied markedly with ischemia and reperfusion.The levels of NO repeatedly increased when the heart was exposed to three episodes of 5-minute;schemia,and were almost completely reversed during each reperfusion period.NO and cGMP levels were significantly different between the 5-minute period of ischemia and the same period of reperfusion during preconditioning.Conclusiona NO plays an important role dudng early phase myocardial ischemic preconditioning in rats.NO and cGMP could be triggers and mediators of early phase myocardial ischemic preconditioning.Altered NOS activity following ischemic stress could be the primary inducer of higher NO levels detected.NO and cGMP fluctuations might be the trigger for protection during early phase myocardial ischemic preconditioning.