BackgroundPrevious studies have demonstrated that heatshock treatment results in the induction of 72-kD heat-shock protein (HSP72) and a reduction of infarct size after subsequent ischemia and reperfusion.Methods and ResultsTo test the hypothesis that the degree of protection from ischemic injury in heat-shocked rats correlates with the degree of prior HSP72 induction, rats pretreated with 40°C, 41°C, or 42°C of whole-body hyperthermia followed by 24 hours of recovery and control rats (n=6 in each group) were quantitatively assessed for the presence of myocardial HSP72 by optical densitometry of Western blots and a primary antibody that is specific for HSP72 and a tertiary antibody labeled with125I. Although rats heat-shocked to 40°C had no significant induction of myocardial HSP72, rats heat-shocked to 41°C and 42°C demonstrated progressively increased amounts of myocardial HSP72 compared with controls. Separate groups of rats heat-shocked to 40°C (n= 16), 41°C (n=37), and 42°C (n=36) with 24 hours of recovery and controls (n=26) were subjected to 35 minutes of left coronary artery occlusion and 120 minutes of reperfusion. Compared with control and 40°C rats, there was progressive infarct size reduction, assessed by triphenyltetrazolium chloride staining, in rats that were heat-shocked to 41°C and 42°C. Furthermore, there was a direct correlation between the amount of HSP72 induced and the reduction in infarct size (r= .97,P= .037).ConclusionsThese results suggest that the improved salvage after heat-shock pretreatment may be related to the amount of HSP72 induced before prolonged ischemia and reperfusion.