• Giuseppe Ristagno, Tong Wang, Wanchun Tang, Shijie Sun, Carlos Castillo, and Max Harry Weil.
• Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA.
• Crit. Care Med. 2008 Nov 1; 36 (11 Suppl): S422-7.

ObjectivesWe examined the effects of energy delivered with electrical defibrillation on myocyte contractility and intracellular Ca2+ dynamics. We hypothesized that increasing the defibrillation energy would produce correspondent reduction in myocyte contractility and intracellular Ca2+ dynamics.DesignRandomized prospective study.SettingUniversity-affiliated research laboratory.SubjectsVentricular myocytes from male Sprague-Dawley rat hearts.Materials And MethodsVentricular cardiomyocytes loaded with Fura-2/AM were placed in a chamber mounted on an inverted microscope and superfused with a buffer solution at 37 degrees C. The cells were field stimulated to contract and mechanical properties were assessed using a video-based edge-detection system. Intracellular Ca2+ dynamics were evaluated with a dual-excitation fluorescence photomultiplier system. Myocytes were then randomized to receive 1) a single 0.5-J biphasic shock; 2) a single 1-J biphasic shock; 3) a single 2-J biphasic shock; and 4) a control group without shock. After the shock, myocytes were paced for an additional 4 mins.ResultsA single 0.5-J shock did not have effects on contractility and intracellular Ca2+ dynamics. Higher energy shocks, i.e., 1- or 2-J shocks, significantly impaired contractility and intracellular Ca2+ dynamics. The adverse effects were greater after a 2-J shock compared with a 1-J shock.ConclusionsHigher defibrillation energy significantly impairs ventricular contractility at the myocyte level. Reductions in cardiomyocyte shortening and intracellular Ca2+ dynamics abnormalities were greater when higher energy shock was used.

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