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 cardioplegia solution is the main determinant of myocyte swelling, and (2) reperfusion myocyte shrinkage results from a rectifying Cl − conductance. M...

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Bibliographic Details
Published inThe Annals of thoracic surgery Vol. 70; no. 2; pp. 633 - 638
Main Authors Sun, Xiwu, Ducko, Christopher T, Hoenicke, Eric M, Reigle, Karen, Damiano, Ralph J
Format Journal Article
LanguageEnglish
Published Netherlands Elsevier Inc 01.08.2000
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Summary:Background. Cardioplegia has been shown to induce significant cell swelling. This study tested the hypothesis that (1) the [K +][Cl −] product of the cardioplegia solution is the main determinant of myocyte swelling, and (2) reperfusion myocyte shrinkage results from a rectifying Cl − conductance. Methods. Rabbit ventricular myocytes were superfused with 37°C Krebs-Henseleit solution for 10 minutes. Then cells underwent 20 minutes of superfusion 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°C. Cells were then resuperfused with 37°C Krebs-Henseleit solution for 30 minutes. Cell volume was measured by videomicroscopy. Results. Cells superfused with St. Thomas’ having [K +][Cl −] products of 2,566, 1,500, and 700 mmol/L 2 swelled by 9.18% ± 3.57%, 5.51% ± 1.08%, and 1.49% ± 1.56%, respectively. Reexposure to Krebs-Henseleit solution caused 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 given at the onset of superfusion. Conclusions. Lowering the [K +][Cl −] product of St. Thomas’ solution attenuated myocyte edema. Myocyte shrinkage during reexposure to Krebs-Henseleit solution resulted from the volume-activated Cl − channel.
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ISSN:0003-4975
1552-6259
DOI:10.1016/S0003-4975(00)01403-X