Hypothermia triggers iron-dependent lipoperoxidative damage in the isolated rat heart.

The extent and time course of recovery on return to normothermia were studied in isolated rat hearts, perfused with oxygen-saturated Tyrode's solution at 5-7 degrees C. After a 1-h hypothermia period, complete recovery was obtained on rewarming; after 3 h hypothermia irreversible deterioration of electrical and mechanical activities resulted. The level of lipid peroxidation, evaluated by the thiobarbituric acid (TBA) reaction, showed a dramatic transient increase on return to normothermia, accompanied by a decrease in the levels of reduced glutathione (GSH). Perfusion with iron chelator-containing saline completely prevented both the deterioration and the peak of lipid peroxidation. These results show that lipid peroxidation is responsible for the cold injury. It is proposed that lipid peroxidation is produced as the result of a cold-induced oxidative stress.