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Ann Thorac Surg 2006;81:148-153
© 2006 The Society of Thoracic Surgeons

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Original article: Cardiovascular

Role of the Sarcolemmal Adenosine Triphosphate–Sensitive Potassium Channel in Hyperkalemic Cardioplegia-Induced Myocyte Swelling and Reduced Contractility

^a Division of Cardiothoracic Surgery, Department of Surgery, Washington University School of Medicine, St. Louis, Missouri
^b Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri

Accepted for publication June 20, 2005.

^_* Address correspondence to Dr Lawton, Washington University School of Medicine, 660 S. Euclid Ave, Campus Box 8234, St. Louis, MO 63110 (Email: lawtonj{at}msnotes.wustl.edu).

BACKGROUND: Hyperkalemic cardioplegia (Plegisol) has been shown to result in myocyte swelling and reduced contractility. We have demonstrated the elimination of these detrimental effects by the addition of an adenosine triphosphate–sensitive K⁺ (K_ATP) channel opener. To examine whether the mitochondrial or sarcolemmal K_ATP channel might be involved, volume and contractility in isolated myocytes from wild-type mice and mice lacking the sarcolemmal K_ATP channel (Kir6.2–/–) were evaluated.

METHODS: Myocytes were perfused for 20 minutes each with control 37°C Tyrode's solution, test solution, and then control solution. Test solutions were (n = 10 per group) either 9°C Plegisol or 9°C Plegisol with 100 µmol/L of diazoxide, a putative mitochondrial-specific K_ATP channel opener. Cell volume and contractility were measured by digital video microscopy at baseline and during the test solution and reexposure periods.

RESULTS: Myocytes from wild-type mice, perfused with 9°C Plegisol, demonstrated significant cell swelling (11.2% ± 0.4%; p < 0.01) and diminished contractility (32.5% ± 9.6% reduction in percent shortening, 47.2% ± 10.1% reduction in peak velocity of shortening, and 52.0% ± 8.8% reduction in peak velocity of relengthening; p < 0.05) versus baseline. Cell swelling and diminished contractility were significantly reduced by the addition of diazoxide. In Kir6.2–/– myocytes, Plegisol caused a greatly reduced level of cell swelling (3.2% ± 0.1%; p < 0.01), and this was unaffected by diazoxide. Contractility was unchanged in Kir6.2–/– myocytes after Plegisol.

CONCLUSIONS: The sarcolemmal K_ATP channel appears necessary for exaggerated cell swelling and reduced contractility to occur after hyperkalemic cardioplegia in mouse myocytes.

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				A. S. Al-Dadah, R. K. Voeller, R. B. Schuessler, R. J. Damiano Jr, and J. S. Lawton Maintenance of Myocyte Volume Homeostasis During Stress by Diazoxide is Cardioprotective Ann. Thorac. Surg., September 1, 2007; 84(3): 857 - 862. [Abstract] [Full Text] [PDF]