Abstract P196: Hypothermia Improves Ventricular Myocyte Sensitivity to Extracellular Ca2+
Background. 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 effects.
Hypothesis. Hypothermia would increase myocyte sensitivity to extracellular Ca2+ under conditions of normal perfusion and following reperfusion after ischemia.
Methods. Myocytes from Sprague-Dawley rat hearts were randomized to be perfused at one of the following extracellular Ca2+ concentrations: 0.5, 1 or 2 mM. Myocytes were further randomized to be perfused at either 37°C or 30°C. A separate group of myocytes was subjected to an initial 10 min interval of ischemia prior to reperfusion at the selected Ca2+ content and temperature. Myocytes were field-stimulated to contract and contractility was assessed using a video-based edge-detection system.
Results. Increases in extracellular Ca2+ content resulted in a positive staircase in myocyte contractility response both at 37°C and 30°C (p<0.02 and p <0.001). However, in myocytes perfused at 30°C, contractility increases in response to increases in extracellular Ca2+ were greater (p <0.001 vs 37°C, Figure A⇓). When myocytes were subjected to ischemia prior to reperfusion, increases in extracellular Ca2+ content led to greater cell contractility during reperfusion at 30°C (p<0.001 vs 37°C, Figure B⇓).
Conclusions. 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.