Mechanisms responsible for cell volume regulation during hyperkalemic cardioplegic arrest

Background. Cardioplegia has been shown to induce significant cell swelling . This study tested the hypothesis that (1) the [K+][Cl-] product of the ca rdioplegia solution is the main determinant of myocyte swelling, and (2) re perfusion myocyte shrinkage results from a rectifying Cl- conductance. Methods. Rabbit ventricular myocytes were superfused with 37 degrees C Kreb s-Henseleit solution for 10 minutes. Then cells underwent 20 minutes of sup erfusion with standard St. Thomas' solution ([K+][Cl-] product = 2566 mmol/ L-2) and two solutions with lower [K+][Cl-] product (1500 and 700 mmol/L-2) at 9 degrees C. Cells were then resuperfused with 37 degrees C Krebs-Hense leit solution for 30 minutes. Cell volume was measured by videomicroscopy. Results. Cells superfused with St. Thomas' having [K+][Cl-] products of 2,5 66, 1,500, and 700 mmol/L-2 swelled by 9.18% +/- 3.57%, 5.51% +/- 1.08%, an d 1.49% +/- 1.56%, respectively. Reexposure to Krebs-Henseleit solution cau sed these cells to shrink by 5.79% +/- 1.41%, 8.72% +/- 3.68%, and 13.46% 5 .60%, respectively. This shrinkage was blocked by Cl- channel blockers give n at the onset of superfusion. Conclusions. Lowering the [K+][Cl-] product of St. Thomas' solution attenua ted myocyte edema. Myocyte shrinkage during reexposure to Krebs-Henseleit s olution resulted from the volume-activated Cl- channel. (C) 2000 by The Soc iety of Thoracic Surgeons.