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Background  A higher increase in intracellular Na +  via Na + /H +  exchanger (NHE) during ischemia has been reported in type 2 diabetic mouse hearts. We investigated the role of NHE in inducing changes in cytoplasmic Ca 2+  concentration ([Ca 2+ ] i ) and alterations in ventricular function during ischemia-reperfusion in type 2 diabetic mouse hearts.    Methods  Hearts from male type 2 diabetic  db/db  (12-15 weeks old) and age-matched control  db/+  mice were subjected to Langendorff perfusion and loaded with 4μM of the Ca 2+  indicator fura-2. The hearts were exposed to no-flow ischemia for 15 minutes and then reperfused. [Ca 2+ ] i  was measured by monitoring fura-2 fluorescence at 500 nm (excitation wavelengths of 340 and 380 nm), while left ventricular (LV) pressure was simultaneously measured.    Results   db/db  hearts exhibited a lower recovery of LV developed pressure than  db/+  hearts during reperfusion following ischemia. Diastolic [Ca 2+ ] i  was increased to a greater level in diabetic hearts than in the control hearts during ischemia and reperfusion. Such an increase in cytoplasmic Ca 2+  overload during ischemia-reperfusion in diabetic hearts was markedly reduced in the presence of the NHE inhibitor cariporide. This was accompanied by a significantly improved recovery of ventricular function on reperfusion, as shown by a lower increase in diastolic pressure and increased recovery of developed pressure.    Conclusion  NHE plays a key role in enhancing cytoplasmic Ca 2+  overload during ischemia-reperfusion and severely impairing post-ischemic cardiac function in hearts from type 2 diabetic  db/db  mice.

The role of Na+/H+ exchanger in Ca2+ overload and ischemic myocardial damage in hearts from type 2 diabetic db/db mice