Objective: To discuss effects and the possible mechanism of noninvasive limb ischemic preconditioning on ischemic myocardial rabbits by observing the expression of heat shock protein 70(HSP70)

cyclooxygen ase-2(COX-2)

inducible nitric oxide synthase(iNOS)

tumour necrosts factor-α(TNF-α)

nudear factor-κB(NF-κB) mRNA and the variation of superaxide(SOD)

malondialdehyde(MDA) and nitric oxide(NO). Method: Rabbits were randomly divided into ischemia control(Ctr)group

non-invasive limb ischemic preconditioning (LIP)group

LIP+KATP antagonist

glibenclamide

(LG)group. In ctr group any special treatment was not performed

but the vasopressin was injected intravenously to produce myocardial ischemia background

then epine-phrine was injected to induce arrhythmia。Double hindlimb ischemia 5 min and reperfusion 5 min was carried out with repetitionof four times to set up a non-invasive limb ischemic preconditioning model. Another methods and contents of observation were same as the Ctr group. The KATP antagonist (glibenclamide) was injected intravenously to LG group rabbits beforehand

another treatments same with the LIP group. After that

SOD

MDA

NO levels in myocardial tissue were detected by biochemistry method; The mRNA expression level of HSP70

COX-2

iNOS

TNF-α and NF-κB was evaluated by RT-PCR. Result: In LIP group COX-2 and iNOS expression level was significantly higher compared with the Ctr group

and TNF-α and NF-κB expression level was significantly reduced;in LG group HSP70 and iNOS expression level was significantly reduced compared with the LIP group

and the TNF-α and NF-κB expression level was significantly increased

and the difference was statistically significant. SOD level in myocardial tissuein LIP group was higher than others

there was no significant difference between Ctr and LIP group; MDA level in Ctr group wasa higher than other groups; NO level in LIP groupwas higher than others

therewas no significant difference between Ctr and LG group. Conclusion: LIP can effectively improve the ischemic myocardial injury

and the KATP pathway may have a very important role in its protective effects.