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J Thorac Cardiovasc Surg 1999;118:123-134
© 1999 Mosby, Inc.

CARDIOTHORACIC TRANSPLANTATION

LONG-TERM MYOCARDIAL PRESERVATION: EFFECTS OF HYPERKALEMIA, SODIUM CHANNEL, AND Na⁺/K⁺/2Cl^- COTRANSPORT INHIBITION ON EXTRACELLULAR POTASSIUM ACCUMULATION DURING HYPOTHERMIC STORAGE

From Cardiac Surgical Research^a and Cardiovascular Research, ^b The Rayne Institute, St Thomas' Hospital, London, United Kingdom.

This study was funded by a PhD Studentship grant from the British Heart Foundation.

Address for reprints: D. J. Chambers, PhD, Cardiac Surgical Research/Cardiothoracic Surgery, The Rayne Institute, St Thomas' Hospital, London, SE1 7EH, United Kingdom.

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 µmol/L) arrest and hypothermic (7.5°C) storage (5 hours), (2) to determine dose-dependent (0.1, 1.0, 10 and 100 µmol/L) effects of the Na ⁺/K⁺/2Cl^- cotransport inhibitor, furosemide, on extracellular K⁺ accumulation during polarized arrest and 7.5°C 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 µmol/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)