Limb Ischemic Preconditioning, Electrical Stimulation Of Femoral Nerve With High Frequency Reduce Infarct Size Following Myocardial Ischemia-reperfusion In Rats

Ischemic preconditioning (IP) was first described by Murry et al in 1986,in which the myocardium could endure injury by exposing it to repeated episodes of transient ischemia-reperfusion before a subsequent sustained ischemia and /or reperfusion. Then many workers demonstrated that remote organ ischemic preconditioning also could protect myocardium from icshemia-reperfusion injury. Investigators pointed out that clarification of the mechanism underlying the cardioprotection by remote organ ischemic preconditioning was not only theoretically important but also clinically valuable. Although several hypotheses on the mechanism have been proposed , and the prevalent opinion is that during remote organ ischemic preconditioning protective mediators such as adenosine, bradykinin and so on were released which could mediated the cardioprotection by activating some nerves. So we examine whether limb ischemic preconditioning can protect myocardium from ischemia-reperfusion injury in anesthetized rats, and define the role of adenosine and nerve. Also by electrostimulating femoral nerve, we observe whether it can afford cardioprotection and the mechanism involved in if it can. The results obtained are as follows:1 Limb ischemic preconditioning reduces infarct size following myocardial ischemia-reperfusion in ratsThe effect of limb ischemic preconditioning(LIP)on ischemia-reperfused myocardium were examined in the urethane-anesthetized rats to determine whether LIP produces cardioprotection and to observe the roles of adenosine and neural reflex in this effect．The area at risk (AR) and infarct area (IA) were determined using Evans blue and nitro-blue tetrazolium staining respectively ．Infarct size (IS) was defined as 100×IA/AR (%)．The results obtained are as follows:(1) During 30 min myocardial ischemia and subsequent 120 min reperfusion, the myocardial infarct size occupied 51.48±0.82% of the area at risk.．(2) LIP significantly reduced the myocardial infarct size to 35.14±0.88% (p<0.01),indicating the cardioprotection effect of such an intervention．(3) Femoral nerve section (FNS) completely abolished the cardioprotection afforded by LIP．(4) Intrafemoral artery injection of adenosine (10nmol/kg) produced similar effect of LIP,reducing the myocardial size to 37.28±1.68%,while intrafemoral vein injection of the same dose of adenosine showed no effect．(5) Pretreatment with a selective adenosine A1 receptor antagonist 8-cyclopentyl-1,diproylxanthine (DPCPX) (32 nmol/kg) partially abolished the cardioprotection of LIP on myocardium ．Taken together, it is concluded that LIP reduces infarct size following myocardial ischemia-reperfusion, and that the locally released adenosine and thereby the activated relevant neural pathway play an important role in the cardioprotection provided by LIP．...