Hypothermia improves ventricular myocyte contractility under conditions of normal perfusion and after an interval 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 10 min interval of ischemia.

Methods

Ventricular myocytes were obtained from 10 male Sprague-Dawley rats weighing 400 ± 50 g. 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 10 min 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. 0.5 mM, 1 mM and 2 mM.

Results

During normal perfusion and following reperfusion after 10 min of ischemia, myocyte contractility increased at 34 °C compared to 37 °C (P < 0.01). When the perfusion temperature was decreased to 32 °C and 30 °C, contractility further increased (P < 0.001). Intracellular Ca²⁺ transients were greater during perfusion at 34 °C compared to those at 37 °C (P < 0.001) and further increased at 30 °C (P < 0.001). Increases in extracellular Ca²⁺ concentration from 0.5 mM to 2 mM resulted in greater myocyte contractility during perfusion at 30 °C compared to that observed at 37 °C (P < 0.001). Effects of hypothermia on intracellular Ca²⁺ 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 10 min of ischemia.