AIMTo investigate a possible role for the transcription factor nuclear factor kappa-B (NF-kappaB) in preconditioning of the heart to ischemia by remote, early protection.

METHODS48 Wistar rats were randomly divided into three experimental groups. In group I/R, the rats underwent 30 min occlusion of the left anterior descending coronary artery, and 120 min reperfusion. In group PL, the rats underwent four cycles of 5 min occlusion and reperfusion of both hind limbs using a tourniquet before the experiment was continued as in Group I/R. In Group P(L-D), we administered NF-kappaB specific inhibitor, ProDTC 125 mg/kg peritoneally, 15 min before IPG. Infarct size as a percentage of the area at risk was determined by triphenyltetrazolium chloride staining. And another 8 rats in each group were killed and myocardium were stored in liquid nitrogen for the measurement of NF-kappaB mRNA.

RESULTSThe myocardial infarct size (IS) was decreased significantly in Group PL compared with group I/R, and the IS/AAR was 34.5% +/- 7.6% and 58.5% +/- 8.5%, respectively ( P < 0.05). The IS/AAR was 54.4% +/- 8.9% in group P(L-D), and there was no significant difference compared with group I/R (P > 0.05). The NF-kappaBmRNA was weaker in P(L) group than that in I/R Group,but is stronger than that in P(L-D) group (P < 0.05). There was almost no expression of NF-kappaB mRNA in P(L-D) group.

CONCLUSIONNoninvasive limb IPC is effective in protecting the myocardium from ischemia reperfusion injury. NF-kappaB plays an important role in the mechanism of this acute remote preconditioning.