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Current Medical Research Programs ?Hypothermic Reperfusion after Ischemia Improves Ventricular Myocyte Contractility and Intracellular Ca2+?Dynamics? An energy-sparing effect of hypothermia has been described, such that lowering the temperature may lead to increases in cardiac work without increases in energy cost. We have recently reportedimproved myocardial function with hypothermia following resuscitation from cardiac arrest. In the present?investigation,we hypothesized that reductions in reperfusion temperature from37°C?to?30°C?after 10 minutes of ischemia would minimize the decreases in myocyte contractility and intracellular Ca2+transients.?Results:?Hypothermic reperfusion following ischemia improved?myocyte contractility.?Increased myocyte?intracellular Ca2+?dynamics during hypothermia accounted for the greater cell contractility. ? Hypothermia Improves Ventricular Myocyte Sensitivity to Extracellular?Ca2+ We have previously reported that hypothermia minimizes the impairment of myocyte contractility following ischemia. In the present?study,?we investigated the mechanisms accounting for these reduced impairments in contractility. We hypothesized that hypothermia would increase myocyte?sensitivity?to?extracellular Ca2+?under conditions of normal perfusion and following reperfusion after ischemia.?Results:?Hypothermia increased myocyte sensitivity to extracellular Ca2+?content, and this accounted for greater contractility.?Hypothermic reperfusion after ischemia maintained greater responsiveness of myocyte contractility to extracellular Ca2+?content, in comparison to normothermic reperfusion. ? ? Current-Based Impedance Compensation Outperformed Duration-Based Technique in Defibrillation Efficacy in a High Impedance Pig Model Transthoracic impedance (TI) for defibrillation varies widely in patients with a median value of approximately 95-100 ohms. High impedance patients are more difficult to defibrillate. The modern generation of external defibrillators ther