Induction of 72-kDa heat shock protein does not produce second window of ischemic preconditioning in rat heart

Ischemic preconditioning (PC) induces delayed phase of protection, known as the second window of protection (SWOP). We investigated this phenomenon in rat and correlated it with the expression of 72-kDa heat shock protein (HS P 72). Rats were preconditioned with 1, 2, and 3 cycles of 5-min left anter ior descending artery occlusions, each separated by a 10-min reperfusion (P C x 1, PC x 2 and PC x 3, respectively). Another group of rats was precondi tioned with heat shock (HS) by raising temperature to 42 degrees C for 15 m in. Twenty-four hours later, rats were given sustained ischemia for 30 min and 90 min of reperfusion. Infarct sizes (%risk area) were 40.0 +/- 7.5, 37 .6 +/- 5.6, and 47.6 +/- 2.4 (mean +/- SE) for PC x 1, PC x 2, and PC x 3 h earts, respectively, which were not different from the sham (49.9 +/- 3.9, P > 0.05). In contrast, infarct size was reduced from 47.5 +/- 3.8% in sham to 4.7 +/- 2.3% (P < 0.01) 24 h after HS. Additionally, early PC significa ntly reduced infarct size from 47.5 +/- 3.8% in controls to 6.0 +/- 1.2 and 5.0 +/- 1.1% nith PC x 1 and PC x 3. Repeated PC cycles induced over a thr eefold increase in HSP 70 mRNA after 2 h compared with sham (P < 0.05). HSP 72, which increased 24 h after PC or HS, was not significantly different b etween the two PC stimuli. We conclude that PC does not induce SWOP in rat heart despite enhanced expression of HSP 72. In contrast, MS-induced delaye d protection was associated with enhanced accumulation of HSP 72. It is pos sible that SWOP and HS have distinct mechanisms of protection that may not be exclusively related to HSP 72 expression.