Hypothermia improves ventricular myocyte contractility under conditions of normal perfusion and after an interval of ischemia.

Abstract

Recent investigations have reported improved myocardial function during hypothermia following resuscitation from cardiac arrest. The effects of hypothermia on myocyte contractility were investigated under conditions of normal perfusion and after a 10min interval of ischemia. Ventricular myocytes were obtained from 10 male Sprague-Dawley rats weighing 400+/-50g. The myocytes were randomized to be perfused at: 37 degrees C, 34 degrees C, 32 degrees C, or 30 degrees C. A subsequent set of myocytes was subjected to 10min of ischemia at 37 degrees C, prior to being randomized to reperfusion at: 37 degrees C, 34 degrees C, 32 degrees C or 30 degrees C. Myocyte contractility was expressed as length-shortening percentage. Intracellular Ca(2+) transients were assessed in a separate group of myocytes preloaded with Fura-2/AM. Sensitivity to Ca(2+) was tested by increasing perfusate Ca(2+) content, i.e. 0.5mM, 1mM and 2mM. During normal perfusion and following reperfusion after 10min of ischemia, myocyte contractility increased at 34 degrees C compared to 37 degrees C (P<0.01). When the perfusion temperature was decreased to 32 degrees C and 30 degrees C, contractility further increased (P<0.001). Intracellular Ca(2+) transients were greater during perfusion at 34 degrees C compared to those at 37 degrees C (P<0.001) and further increased at 30 degrees C (P<0.001). Increases in extracellular Ca(2+) concentration from 0.5mM to 2mM resulted in greater myocyte contractility during perfusion at 30 degrees C compared to that observed at 37 degrees C (P<0.001). Effects of hypothermia on intracellular Ca(2+) transients and sensitivity to Ca(2+) persisted after ischemia. Hypothermia improved myocyte contractility, intracellular Ca(2+) transients and sensitivity to Ca(2+) under conditions of normal perfusion and following reperfusion after 10min of ischemia.