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 10. min 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°C, 34°C, 32°C, or 30°C. A subsequent set of myocytes was subjected to 10min of ischemia at 37°C, prior to being randomized to reperfusion at: 37°C, 34°C, 32°C or 30°C. Myocyte contractility was expressed as length-shortening percentage. Intracellular Ca2+ transients were assessed in a separate group of myocytes preloaded with Fura-2/AM. Sensitivity to Ca2+ was tested by increasing perfusate Ca2+ content, i.e. 0.5mM, 1mM and 2mM. Results: During normal perfusion and following reperfusion after 10min of ischemia, myocyte contractility increased at 34°C compared to 37°C (P2+ transients were greater during perfusion at 34°C compared to those at 37°C (P2+ concentration from 0.5mM to 2mM resulted in greater myocyte contractility during perfusion at 30°C compared to that observed at 37°C (P2+ transients and sensitivity to Ca2+ persisted after ischemia. Conclusions: Hypothermia improved myocyte contractility, intracellular Ca2+ transients and sensitivity to Ca2+ under conditions of normal perfusion and following reperfusion after 10min of ischemia.
|Number of pages||6|
|Publication status||Published - Jul 2010|
- Intracellular Ca
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Emergency Medicine