| ObjectiveTo study the effects and differences of noninvasive early and delayed limbischemic preconditioning(NLIPC) against myocardial ischemia-reperfusion injury inrats with heart failure.Method70healthy male SD rats were randomly divided into normal group (n=10) andheart failure group (n=60). The rats in heart failure group were induced heartfailure by partial coarctation of abdominal aorta. Normal group were not acceptedany treatment.The12th week after operation, the rats in heart failure group weretaken ultrasonic cardiogram to validate whether be induced to heart failure.The heartfailure rats were randomly divided into4groups:(1) sham operation (Sham) group:rats were threaded a silk suture under the left coronary artery anterior descending(LAD) and laid up throughout the experiment for150min,not tensioned;(2)ischemia/reperfusion (I/R) group: rats were subjected to30min LAD occlusionfollowed by120minutes reperfusion;(3) noninvasive early limb ischemicpreconditioning (NELIPC) group: rats were subjected to three episodes of5minischemia of left hind limb followed by5min reperfusion, then30min ischemiafollowed by120min reperfusion of LAD was immediately performed;(4)noninvasive delayed limb ischemic preconditioning (NDLIPC) group: rats weresubjected to three episodes of5min ischemia of left hind limb followed by5minreperfusion,24hours later,30min ischemia followed by120min reperfusion ofLAD was performed.Collect venous blood before the LAD ligated and at120minutes of reperfusion.Detect the serum content of creatine kinaseisoenzyme(CK-MB) and cardiac troponin I (cTnI) with the use of automatic biochemistry analyzer.Detect the activity of superoxide dismutase (SOD) and theserum content of malondialdehyde (MDA) in by ELISA. Myocardial infarct size wasdetermined based on2,3,5-triphenyltetrazodium chloride staining.Results1.The heart function of the heart failure group was obviously lower than thenormal group,it was showed as the LVEDD of heart failure group was significantlyincreased compared with normal group(7.57±0.41mm vs6.07±0.32mm, p<0.01),theLVESD of heart failure group was significantly increased compared with normalgroup (5.57±0.41mm vs3.05±0.29mm, p<0.01).The LVEF of heart failure group wassignificantly decreased compared with normal group(30.8±6.1%vs63.7±4.9%,p<0.01).The heart failure model was successful established.2.The serum content of CK-MB,cTnI,MDA and activity of SOD had nosignificant difference among each group before LAD ligated(p<0.01). At120minuters of reperfusion, compared with I/R group: the amplitude of increase of theserum content of CK-MB、cTnI、MDA were reduced in the NELIPC group andNDLIPC group(p<0.01)，the NELIPC group decreased more obviously than NDLIPCgroup（p<0.05）；the amplitude of decrease of the serum activity of SOD werereduced in the NELIPC group and NDLIPC group(p<0.01，p<0.05)，the NELIPCgroup decreased more obviously than NDLIPC grou（pp<0.05）；the myocardial infarctsize was decreased in the NELIPC group and NDLIPC group(p<0.01), the NELIPCgroup decreased more obviously than NDLIPC group(p<0.01).Conclusion1.NLIPC can reduce the release of cTnI、CK-MB,reduce myocardial infarct size,reduce the damage and necrosis of myocardial cells；decrease the content of MDA inserum, increase the activity of SOD, enhance antioxidative ability of myocardiumduring myocardial ischemia/reperfusion in rats with heart failure，has protective effecton myocardial ischemia/reperfusion injury of heart failure.2.The early protective effect of NLIPC on myocardial ischemia/reperfusioninjury in rats with heart failure is better than the delayed protective effect of NLIPC. |
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