Abstract: AIM: To study the role of Na⁺-K⁺-ATPase in the protective mechanism of ischemic preconditioning (IP) on myocardial ischemia and reperfusion injury. METHODS: Ligation of anterior descending branch of rat hearts for 30 min (ischemia) and reperfusion for 60 min were for establishing the model of ischemia reperfusion (I R), and 5 min of ischemia and 10min of reperfusion were made for three cycles with a view to preparing IP model.After hemodynamic data were recorded, myocardium sample was processed immediately in order to measure the activity of Na⁺-K⁺-ATPase and Ca₂⁺-Mg₂⁺-ATPase and the changes of protein expression of α1, α2,α3 and β1 isoforms of Na⁺-K⁺-ATPase. RESULTS: IRreduced cardiac contractile and diastolic function, activityof Na⁺-K⁺-ATPase and Ca₂⁺-Mg₂⁺-ATPase, and protein expression of α1, α2, α3 and β1 isoforms of Na⁺-K⁺-ATPase.IP attenuated the reduction of cardiac function, the activities and protein expression of Na⁺-K⁺-ATPaseα1, α2, α3 and β1-isoforms induced by I R.Digilanid Cabolished the effects of IP on Na⁺-K⁺-ATPase. CONCLUSION: The beneficial effects of IP on the prohibition of Na⁺-K⁺-ATPase induced by myocardial ischemia and reperfusion were abolished by cardiac glycoside.ProtectingNa⁺-K⁺-ATPase may play an important role in the mechanism of IP.

Key words: ischemic preconditioning, myocardium, Na⁺-K⁺-ATPase gene expression, digilanid C