Background Endogenous nitric oxide and adenosine increase simultaneously to keep the balance of energy demandand supply when the oxygen supply is insufficient,which suggests that nitric oxide and adenosine might exert asynergistic myoprotection during tissue hypoxia.In this study,we tested this hypothesis utilizing a canine model ofprolonged global myocardial ischaemic reperfusion injury.Methods In this double blind,controlled study,the hearts of 24 anaesthetized mongrel dogs were arrested for 2 hourswith aortic cross clamping and blood cardioplegia.The treatment groups were those supplemented with 2 mmol/LL-arginine(ARG),supplemented with 1 mmol/L adenosine(ADO),ARG+ADO supplemented with both,and nosupplementation(control)(n=6 in each group).Haemodynamics,biochemical indices,adenosine triphosphate(ATP)content and myeloperoxidase activities of myocardium were determined to evaluate myocardial injury.Statisticalcomparison was performed by two way ANOVA.Results Although the requirements for inotropic supports were higher,the cardiac outputs were lower in control groupthan in ARG,ADO and the combination groups.Plasma cardiac troponin I levels were higher and the areas of hydropicchanges were larger in control group than in ARG and ADO groups.Combination of arginine and adenosine providedfurther myoprotection with respect to better cardiac performance,lower release of cardiac troponin I,and smaller areas ofhydropic changes compared with ARG and ADO groups.ATP content was higher,but myeloperoxidase activities ofmyocardium were significantly lower in the combination group than in control,ARG and ADO groups(P<0.05).Conclusions Combination of L-arginine and adenosine provides synergistic myoprotection in a canine model of globalmyocardial ischaemia.Thus,the combination is recommended when the heart is exposed to a prolonged ischaemiaduring cardiac surgery. Background Endogenous nitric oxide and adenosine increase simultaneously to keep the balance of energy demand and supply when the oxygen supply is insufficient, which suggests that nitric oxide and adenosine might exert asynergistic myoprotection during tissue hypoxia. In this study, we tested this hypothesis utilizing a canine model Ofprolonged global myocardial ischaemic reperfusion injury. Methods In this double blind, controlled study, the hearts of 24 anaesthetized mongrel dogs were arrested for 2 hours with aortic cross clamping and blood cardioplegia. Treatment groups were those supplemented with 2 mmol / LL-arginine (ARG supplemented with 1 mmol / L adenosine (ADO), ARG + ADO supplemented with both, and nosupplementation (control) (n = 6 in each group) .Hemodynamics, biochemical indices, adenosine triphosphate (ATP) content and myeloperoxidase activities of myocardium were determined to evaluate myocardial injury. Statistical comparison was performed by two way ANOVA. Results Although the requirements for inotropic supports were higher, the cardiac outputs were lower in control groupthan in ARG, ADO and the combination groups. Plasma cardiac troponin I levels were higher and the areas of hydropicchanges were larger in control group than in ARG and ADO groups. Combine of arginine and adenosine providedfurther myoprotectionwith respect to better cardiac performance, lower release of cardiac troponin I, and smaller areas ofhydropic changes compared with ARG and ADO groups. ATP content was higher, but myeloperoxidase activities ofmyocardium were significantly lower in the combination group than in control, ARG and ADO groups (P <0.05) .Conclusions Combination of L-arginine and adenosine provides synergistic myoprotection in a canine model of globalmyocardial ischaemia. Thus, the combination is recommended when the heart is exposed to a prolonged ischaemiaduring cardiac surgery.