Preservation of heat stress induced myocardial hsp 72 in aged animals following caloric restriction.

The major stress inducible Heat Shock Protein (HSP 72) confers myocardial protection from ischemia. A decreased ability to express HSP 72 during homeostatic disruptions has been suggested as a possible mechanism for the increased susceptibility of aged hearts to ischemic stress. Given that Caloric Restriction (CR) has been reported to reverse or delay age-associated cellular senescence, we examined the effect of CR on the ability of aged hearts to induce and accumulate HSP 72. Adult (6 months), aged (22 months) and CR aged (22 months) Fisher 344 rats were heat stressed by raising core temperature to 41 degrees C for 10 min. Immediately after heat stress, or 24 h later, the myocardium was examined for either activation of the heat shock transcription factor (HSF) or HSP 72 accumulation. Hearts from heat stressed CR animals demonstrated an increased HSF activation and an increased HSP 72 content when compared to hearts from heat stressed aged animals. The HSF response and HSP 72 content of the hearts from heat stressed aged CR animals was comparable to that observed in hearts from heat stressed adult animals. These results suggest CR may preserve the ability of the aged myocardium to activate and/or express HSP 72.