Abstract P90: Hypothermic Reperfusion After Ischemia Improves Ventricular Myocyte Contractility and Intracellular Ca2+ Dynamics
Background. 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 reported improved myocardial function with hypothermia following resuscitation from cardiac arrest. In the present investigation, we hypothesized that reductions in reperfusion temperature from 37°C to 30°C after 10 minutes of ischemia would minimize the decreases in myocyte contractility and intracellular Ca2+ transients.
Methods. Ventricular myocytes were obtained from Sprague-Dawley rat hearts. After a 10 min interval of ischemia at 37°C, the cells were randomized to receive the perfusate at one of the following temperatures: 37°C, 34°C, and 30°C. Myocytes were field-stimulated to contract and contractility was assessed using a video-based edge-detection system. Intracellular Ca2+ dynamics were evaluated with a dual-excitation fluorescence photomultiplier system in a separate group of myocyte preloaded with Fura-2/AM.
Results. Following reperfusion after 10 mins of ischemia, decreases in the perfusate temperature yielded corresponding increases in myocyte contractility and intracellular Ca2+ transients in comparison to normothermic reperfusion (p<0.001, Figures A and B⇓).
Conclusions. Hypothermic reperfusion following ischemia improved myocyte contractility. Increased myocyte intracellular Ca2+ dynamics during hypothermia accounted for the greater cell contractility.