Background We examined the effects of pinacidil on contractile function and intracellular calcium in isolated rat cardiomyocytes exposed to cardioplegic solution. Methods Rat myocytes were incubated at 24°C for 2 hours in cardioplegic solution with or without pinacidil (50 μmol/L), then they were perfused with Krebs-Henseleit solution with a gas phase of 95% O2/5% CO2 at the same temperature. Contraction and intracellular calcium transients were then measured by video tracking and spectrofluorometry. Results During 20 minutes of perfusion after 2 hours in cardioplegic solution with pinacidil, (1) the recovery of contractile function was significantly increased in terms of both amplitude of contraction (98.30% ± 9.90% versus 81.00% ± 11.25%; p < 0.05) and peak velocity of cell shortening (100.90% ± 13.79% versus 76.89% ± 18.14%; p < 0.01) when compared with myocytes in cardioplegic solution without pinacidil; (2) the amplitudes of the intracellular calcium transients evoked by electrical stimulation and caffeine (10 mmol/L) increased by 23.31% to approximately 40.72% and 61.73%, respectively, compared with those in cardioplegic solution without pinacidil; and (3) the decay time of the caffeine-induced intracellular calcium transient decreased by 36.64% ± 15.10% relative to that measured in cardioplegic solution without pinacidil. The effects induced by supplementing the cardioplegic solution with pinacidil were diminished in the presence of glibenclamide (10 μmol/L). Conclusions Addition of the adenosine triphosphate-sensitive potassium-channel opener, pinacidil, to a high potassium cardioplegic solution improves recovery of contractile properties and cytosolic calcium in isolated rat cardiac myocytes. © 2004 by The Society of Thoracic Surgeons.
Lin, R., Zhang, Z. W., Xiong, Q. X., Cao, C. M., Shu, Q., Bruce, I. C., & Xia, Q. (2004). Pinacidil improves contractile function and intracellular calcium handling in isolated cardiac myocytes exposed to simulated cardioplegic arrest. Annals of Thoracic Surgery, 78(3), 970–975. https://doi.org/10.1016/j.athoracsur.2004.03.084