AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.
AIM: 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. METHODS: 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. RESULTS: 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. CONCLUSIONS: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.
Authors: Jing Li; Michael Fettiplace; Sy-Jou Chen; Benjamin Steinhorn; Zuohui Shao; Xiangdong Zhu; Changqing Li; Shaun Harty; Guy Weinberg; Terry L Vanden Hoek Journal: Crit Care Med Date: 2014-12 Impact factor: 7.598