DISSOCIATION OF HEAT-SHOCK PROTEINS EXPRESSION WITH ISCHEMIC TOLERANCE BY WHOLE-BODY HYPERTHERMIA IN RAT-HEART

Heat shock (HS) results in the expression of heat shock proteins (hsp) and confers tolerance against subsequent ischemic injury. We examined the extent of myocardial protection in vivo, and determined the level of hsp expression induced by HS as a function of time. Anesthetized r ats were subjected to HS by raising core temperature to 42 degrees C f or 15 min and they were then allowed to recover from 2 to 30 h (n = 8- 11 for each time point). At the appropriate time, animals were subject ed to 30 min of ischemia via ligation of the LAD, followed by 90 min o f reperfusion, Infarct size was determined by tetrazolium staining and hsp expression was assessed by Western blots. Following ischemia/repe rfusion, the infarct sizes (% risk area) were 51.3 +/- 3.7, 41.0 +/- 7 .7, 48.0 +/- 6.9 after 2, 4 and 12 h of HS, which were not significant ly different from 39.2 +/- 2.75 in non beat-shocked animals (P > 0.05) . In contrast, the infarct size was reduced significantly to 11.0 +/- 3.1% in 24 h HS group (P < 0.01 v non-heat-shocked control, 2, 4 and 1 2 h HS groups), but increased back to 40.0 +/- 3.2% (P < 0.01) by 30 h after HS. No major significant differences in the mean arterial blood pressure, heart rate or rate pressure product was observed between di fferent groups, The synthesis of 72- and 27-kD hsp in HS groups was ra pid, reaching >80% of maximum within 4 h of initial insult and peaked by 12 h, whereas the protective effect of HS was absent at these time points. Mie conclude that ischemic tolerance afforded by HS cannot be solely explained on the basis of hsp expression, and may be dependent on factors such as post-translational modifications, translocation of hsps or some other as yet unidentified factors. (C) 1998 Academic Pres s.