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Objectives: We previously demonstrated improved myocardial preservation with polarized (tetrodotoxin-induced), compared with depolarized (hyperkalemia-induced), arrest and hypothermic storage. This study was undertaken to determine whether polarized arrest reduced ionic imbalance during ischemic storage and whether this was influenced by Na^+/K ^+/2Cl^- cotransport inhibition. Methods: We used the isolated crystalloid perfused working rat heart preparation (1) to measure extracellular K^+ accumulation (using a K^+-sensitive intramyocardial electrode) during ischemic (control), depolarized (K^+ 16 mmol/L), and polarized (tetrodotoxin, 22 @mmol/L) arrest and hypothermic (7.5^oC) storage (5 hours), (2) to determine dose-dependent (0.1, 1.0, 10 and 100 @mmol/L) effects of the Na ^+/K^+/2Cl^- cotransport inhibitor, furosemide, on extracellular K^+ accumulation during polarized arrest and 7.5^oC storage, and (3) to correlate extracellular K^+ accumulation to postischemic recovery of cardiac function. Results: Characteristic triphasic profiles of extracellular K^+ accumulation were observed in control and depolarized arrested hearts; a significantly attenuated profile with polarized arrested hearts demonstrated reduced extracellular K^+ accumulation, correlating with higher postischemic function (recovery of aortic flow was 54% +/-4% [P = .01] compared with 39% +/-3% and 32% +/-3% in depolarized and control hearts, respectively). Furosemide (0.1, 1.0, 10, and 100 @mmol/L) modified extracellular K^+ accumulation by -18%, -38%, -0.2%, and +9%, respectively, after 30 minutes and by -4%, -27%, +31%, and +42%, respectively, after 5 hours of polarized storage. Recovery of aortic flow was 53% +/-4% (polarized arrest alone), 56% +/-8%, 70% +/-2% (P = .04 vs control), 69% +/-4% (P = .04 vs control), and 65% +/-3% ( P = .04 vs control), respectively. Conclusions: Polarized arrest was associated with a reduced ionic imbalance (demonstrated by reduced extracellular K^+ accumulation) and improved recovery of cardiac function. Further attenuation of extracellular K ^+ accumulation (by furosemide) resulted in additional recovery. (J Thorac Cardiovasc Surg 1999;118:123-34)