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Relative contributions of Na⁺/H⁺ exchange and Na⁺/HCO₃^– cotransport to ischemic Na_i⁺ overload in isolated rat hearts

¹Interuniversity Cardiology Institute of the Netherlands and ²Department of Cardiology, Heart Lung Center Utrecht, University Medical Center, Utrecht, The Netherlands

Submitted 24 November 2003 ; accepted in final form 11 August 2004

The Na⁺/H⁺ exchanger (NHE) and/or the Na⁺/HCO₃^– cotransporter (NBC) were blocked during ischemia in isolated rat hearts. Intracellular Na⁺ concentration ([Na⁺]_i), intracellular pH (pH_i), and energy-related phosphates were measured by using simultaneous ²³Na and ³¹P NMR spectroscopy. Hearts were subjected to 30 min of global ischemia and 30 min of reperfusion. Cariporide (3 µM) or HCO₃^–-free HEPES buffer was used, respectively, to block NHE, NBC, or both. End-ischemic [Na⁺]_i was 320 ± 18% of baseline in HCO₃^–-perfused, untreated hearts, 184 ± 6% of baseline when NHE was blocked, 253 ± 19% of baseline when NBC was blocked, and 154 ± 6% of baseline when both NHE and NBC were blocked. End-ischemic pH_i was 6.09 ± 0.06 in HCO₃^–-perfused, untreated hearts, 5.85 ± 0.02 when NHE was blocked, 5.81 ± 0.05 when NBC was blocked, and 5.70 ± 0.01 when both NHE and NBC were blocked. NHE blockade was cardioprotective, but NBC blockade and combined blockade were not, the latter likely due to a reduction in coronary flow, because omission of HCO₃^– under conditions of NHE blockade severely impaired coronary flow. Combined blockade of NHE and NBC conserved intracellular H⁺ load during reperfusion and led to massive Na⁺ influx when blockades were lifted. Without blockade, both NHE and NBC mediate acid-equivalent efflux in exchange for Na⁺ influx during ischemia, NHE much more than NBC. Blockade of either one does not affect the other.

Na⁺/H⁺ exchanger; cariporide; Na⁺-HCO₃^– cotransporter; ²³Na nuclear magnetic resonance spectroscopy; ischemia

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