Biphasic Effect of Heat Stress Pretreatment on Ischemic Tolerance of Isolated Rat Hearts

Improvement of post-ischemic cardiac function 24 h after heat stress has been attributed to the increased cardiac tissue content of the inducible heat stress protein hsp70. Previous studies indicated that hsp70 is already significantly upregulated a few hours after heat stress. To delineate the relationship between hsp70 tissue content and heat stress-induced cardioprotection in the early time frame after heat stress, if any, post-ischemic functional recovery of isolated, ejecting rat hearts and the actual cardiac hsp70 content were investigated 0.5, 3, 6 and 24 h after heat stress (42 degrees C for 15 min). Recovery (% of pre-ischemic value) of cardiac output, left ventricular developed pressure, and positive and negative left ventricular dP/dtmax was studied during reperfusion after 45 min of global ischemia. Anesthetized non heat-stressed rats served as controls. The recovery of all hemodynamic variables was significantly worse in hearts isolated 30 min after heat stress than in control hearts. When the time interval between heat treatment and the ischemic episode was prolonged, a gradual improvement of post-ischemic functional recovery was observed. Only 24 h after heat treatment functional recovery was significantly better in the heat-stressed than in the control group. Compared to control hearts (0.27+/-0.10 mg/g total protein) cardiac hsp70 content was already significantly increased 0.5 h after heat stress (0.51+/-0.03 mg/g total protein). The cardiac hsp70 content further increased to 0. 70+/-0.11, 0.89+/-0.35 and 1.01+/-0.25 mg/g total protein, at 3, 6 and 24 h after heat stress, respectively. The present findings clearly show that heat stress is associated with a fast rise in the myocardial hsp70 content which, however, is not uniquely correlated with improved ischemia tolerance of the treated hearts, which only occurs 24 h later.