ISCHEMIC PRECONDITIONING ELEVATES CARDIAC STRESS PROTEIN BUT DOES NOTLIMIT INFARCT SIZE 24 OR 48 H LATER IN RABBITS

We investigated whether ischemic preconditioning (PC) produced a secon d window of protection by delayed synthesis of cardioprotective protei ns. Anesthetized open-chest rabbits were subjected to 30 min of corona ry occlusion and 3 h of reperfusion. PC was elicited by 5 min of ische mia and was separated from sustained ischemia by 5 min, 2 h, or 24 h o f reperfusion. Infarct size (% area at risk) was markedly limited by P C with 5 min of reperfusion when compared with controls (13.3 +/- 2.5 vs. 46.8 +/- 7.0%; P < 0.05). This protective effect was lost when the interval between PC and sustained ischemia was extended to 2 h (47.8 +/- 4.8%; P = NS vs. control) and did not reoccur even when it was ext ended to 24 h (44.2 +/- 6.5%; P = NS vs. sham-operated control). To po tentiate induction of heat shock proteins (HSPs), a PC protocol involv ing four 5-min episodes of ischemia and reperfusion was also used and was separated from sustained ischemia by 24 or 48 h of reperfusion. Ho wever, neither of these protocols was protective, and limitation of in farct size was not observed (55.5 +/- 5.9 and 53.4 +/- 6.5% in 24 and 48 h of reperfusion, respectively; P = NS vs. corresponding sham-opera ted control). Myocardial expression of HSPs was examined using a monoc lonal antibody against 72- to 73-kDa HSP in additional rabbits. Immuno reactivity was observed in the myocardium at 24 and 48 h after PC, but not immediately after PC. In conclusion, infarct size-limiting effect of PC was short Lived (<2 h), and a second window of protection was n ot detected even though stress protein synthesis was increased 24 or 4 8 h after PC.