Cardioprotection is strain dependent in rat in response to whole body hyperthermia

Previous results showed a genetic component to cardioprotection. Therefore, we investigated the heat shock response in Wistar and Sprague-Dawley (SD) rats at 24 and 48 h. Rats were subjected to whole body hyperthermia achievi ng colonic temperatures of 40 or 42 degreesC for 20 min. After recovery hea rts were excised for protein measurements or were subjected to 30 min of is chemia and then 2 h of reperfusion. Heat shock protein (HSP) expression was determined by Western blotting and infarct size was determined by tripheny ltetrazolium staining. All groups of SD and Wistar rats demonstrated HSP72 and HSP90 induction at both time points in response to a heat stress of 42 degreesC. At 24 h there was only a significant reduction in infarct size se en in control vs. small SD (60.0 +/- 4.8 vs. 26.5 +/- 2.3) rats. However, a t 48 h control versus small SD (60.0 +/- 4.8 vs. 17.6 +/- 3.8) and Wistar ( 59.4 +/- 4.3 vs. 29.8 +/- 6.0) and control versus large SD (53.7 +/- 2.6 vs . 19.8 +/- 4.7) and Wistar (57.3 +/- 1.6 vs. 34.5 +/- 2.8) rats demonstrate d a significant reduction in infarct size with a greater reduction observed in SD rats. We conclude that heat shock-induced cardioprotection in rats i s dependent on strain, temperature, time after stress, and size.