Preservation of myocyte contractile function after hypothermic cardioplegic arrest by activation of ATP-sensitive potassium channels

• Published in: Circulation (New York, N.Y.) N.Y.), 1997-10, Vol.96 (7), p.2376-2384
• Main Authors: DORMAN, B. H, HEBBAR, L, HINTON, R. B, ROY, R. C, SPINALE, F. G
• Format: Article
• Language: English
• Subjects: Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy; Biological and medical sciences; Emergency and intensive cardiocirculatory care. Cardiogenic shock. Coronary intensive care; Intensive care medicine; Medical sciences
• ISSN: 0009-7322; 1524-4539
• DOI: 10.1161/01.CIR.96.7.2376

Background Left ventricular (LV) dysfunction can occur after hyperkalemic cardioplegic arrest and subsequent reperfusion and rewarming. Activation of adenosine triphosphate (ATP)-sensitive potassium (K atp ) channels within the myocyte sarcolemma has been shown to be cardioprotective for myocardial reperfusion injury and ischemia and may play a contributory role in preconditioning for cardioplegic arrest. Accordingly, the present study tested the hypothesis that cardioplegic arrest and activation of K atp channels by a potassium channel opener (PCO) would attenuate alterations in ionic homeostasis and improve myocyte contractile function. Methods and Results Porcine LV myocytes were isolated and randomly assigned to the following treatment groups: normothermic control, incubation in cell culture media for 2 hours at 37°C (n=60); hyperkalemic cardioplegia, incubation for 2 hours in hypothermic hyperkalemic cardioplegic solution (n=60); or PCO/cardioplegia, incubation in cardioplegic solution containing 100 μmol/L of the PCO aprikalim (n=60). Hyperkalemic cardioplegia and rewarming caused a significant reduction in myocyte velocity of shortening compared with normothermic control values (33±2 versus 66±2 μm/s, P