The protective effect of lowered temperature on the oxygen paradox in the rat heart

The isolated rat heart was completely protected against creatine kinase (CK) release in the standard Ca2+ or O2 paradoxes when perfused at 28 degrees C instead of 37 degrees C, as previously reported. Hearts subjected to the O2 paradox at 28 degrees C recovered normal contractile activity, and electron microscopy revealed normal, undamaged ultrastructure. The mitochondria remained contracted and showed no signs of Ca2+ uptake following a rise in Ca2+ concentration in the cytosol that would be expected following the prolonged period of anoxia. It is concluded that the rise in [Ca2+]i that results from a perturbation of Ca2+ homeostasis during anoxic perfusion in the O2 paradox is not sufficient to cause either CK release or myofilament degradation which follow only on reoxygenation in the second phase of the paradox. Since both the Ca2+ and O2 paradoxes are completely protected when the first stage is carried out at 28 degrees C, it is concluded that the initial activation of the sequence of damage events is prevented at this temperature.