Phosphorylation state of Akt in the heart during artificial deep hypothermia in Syrian hamsters.

Hibernating animals show a remarkable decrease in body temperature without accompanying serious organ damage. Active hypometabolism may be involved in the protective mechanisms. Therefore, in the present study, the phosphorylation status of Akt was used to examine whether metabolism is actively reduced during artificial hypothermia in hamsters. Hypothermia induced by activation of the central adenosine A1 receptor (A1AR) resulted in dephosphorylation of Akt in the heart, as in that of hibernating hamsters. Since phosphorylated Akt almost totally disappeared, it is probable that cellular metabolism is actively reduced in A1AR-mediated hypothermia. Surprisingly, phosphorylation of Akt was significantly, but not totally, reduced even when hypothermia was induced by a combination of inhalation anesthesia and cooling. It can thus be considered that active regulation for the reduction of metabolic activity occurs in A1AR-mediated hypothermia as well as in anesthesia-induced hypothermia, though to a lesser extent. In both hypothermic conditions, serious arrhythmias were rarely observed. In anesthesia-induced hypothermia, during which dephosphorylation of Akt occurred only partially, there was no obvious organ damage in histopathological examination. Taken together, our findings suggest that artificial hypothermia causes active hypometabolism and has therapeutically applicable properties.