| Objective:To study the Ischemic/Reperfusion（I/R） model on the basis of establishing SDrat model of heart failure and Remote Ischemic Preconditioning （RIPC）model.Detection of RIPC on SD rat heart failure before and after myocardial ischemiareperfusion injury, the expression of ET-1and NO changes in serum andelectrocardiogram (ECG) changes, and the morphological changes of myocardial cells,the study RIPC role in SD rats with heart failure, myocardial I/R injury protection.Method:19SD rats succeed into the group, divided into three groups: normal group(n=5)，heart failure group (n=7) and RIPC group (heart failure,n=7).All rats carriedout LAD ischemic30min and reperfusion later.Observed in the process of themyocardial ischemia30min of three groups of SD rat ECG changes, collected indifferent stages of the three groups rats experiment (prior to myocardial ischemia,30min after ischemia and reperfusion after2h) of venous blood, serum specimens afterhigh speed centrifugation, collected reperfusion of myocardial tissue after2h.ELISAmethod is applied to detect ET-1、NO expressed in different stage in the serum,hematoxylin-eosin (Haematoxylin-eosine HE) dyed myocardial tissue electronmicroscope (400times) to observe the morphological changes of myocardial cellsafter three groups. Analysis of RIPC to SD rats with heart failure, myocardial I/Rinjury the relationship between the protection mechanisms. Results:1In the process of the ischemia of three groups of SD rat ECG changes:1.1after LAD ligation, HR are progressive decline in three group, ischemia30min fell to the lowest at the end of a reduced by about10%in the past ligation (P <0.01). Open after reperfusion, HR has increased, but until the end of the120min,failed to return to the front of the ligation (P <0.05). Between the three groups wereno significant differences of each point in time of HR.1.2After LAD ligation in the3-5min, ST-segment in three groups weresignificantly elevated (P <0.01),30min end of the peak. In this case the heart failuregroup ST-segment height is about10times before the ligation, ST-segment in theRIPC group height of6.5before ligation. Compared with the heart failure group, thespeed slows ST-segment elevation RIPC group ischemia, elevated magnitude lower (P<0.01).1.3During the period of ischemia, the heart failure group and RIPC group theincidence of ventricular arrhythmias significantly increased (P <0.05). RIPC groupcompared with the heart failure group, the LAD ligated ventricular premature beat(VPC) in time delayed nearly1times, shorten the duration by50%(P <0.01), theincidence of VPC almost one-third lower (P <0.01); Ventricular tachycardia (VT) intime delayed nearly1times, shorten the duration by50%(P <0.05), reduce theincidence of1/2(P <0.01).2The expression in serum levels of ET-1and NO in the process of I/R2.1Reperfusion after120min, the normal group and heart failure groupsignificantly increased serum concentration of ET-1,1.8times before is LAD ligation(p <0.05), and serum concentration of ET-1RIPC group was1.3times before theLAD ligation (p <0.05). Compared with before ligation, the heart failure group ratsserum concentration of ET-1increased by72%(p <0.01), RIPC group has alsoincreased significantly, but the heart failure group decreased about26%(p <0.01).2.2Before LAD ligation, NO concentration in rat serum RIPC group than in thenormal group and the heart failure group were significantly higher (P <0.05).120min after reperfusion, NO concentration three groups were significantly lower (P <0.01),the heart failure group decreased by73%. Compared with the heart failure group,RIPC serum NO concentration is improved12%(P <0.05).2.3Before ligation, myocardial ischemia30min late, normal group and the heartfailure group ET-1/NO no significant difference in the ratio, while the RIPC serumET-l/NO ratio less than30%in the heart failure group (p <0.05), compared with thepre-ligation,120min late reperfusion significantly increased serum ET-1/NO ratio ofthree groups (p <0.01).ET-1/NO ratio was ligated7.0times in heart failure groupcompared with pre-ligation. While RIPC group compared with the heart failure groupthe ratio of serum ET-1/NO reduced by about50%, decreased the increasingamplitude (P <0.01).3Taking three late120min reperfusion myocardial HE staining, normal: cardiacstriated muscle fibers clearer, a small bundle fracture, most cardiac cell membraneintegrity, cytoplasmic mildly cloudy, mild eosinophilic staining, the majority ofmyocardial nuclear membrane clear, occasionally leaking a small amount red bloodcells, moderate inflammatory cell infiltration. in the heart failure group: aftermyocardial I/R cardiac striated muscle fibers disappear bundle fracture, mostincomplete myocardial cell membrane, cytoplasm cloudy, eosinophilic stainingdeepened, some nuclei dissolved disappeared or were fragmented, interstitialcongestion seen a lot of bulk exudation and inflammatory cell infiltration in the redblood cells. RIPC group: cardiac striated muscle fibers still clear, a small amount ofstriated disappear bundle fracture, most of myocardial cell membrane integrity,cytoplasmic moderate turbidity, moderate eosinophilic dye, dissolve a small nucleusdisappeared hyperemia stromal cells, red blood oozing few scattered and moderateinflammatory cell infiltration.Conclusion:1RIPC can significantly lower the occurs rate and level of ventriculararrhythmias in rats with heart failure during the ischemia. 2RIPC can maintain serum during I/R balance between NO and ET-1, close tothe basic state, stable the function of the vascular endothelium, thus protecting heartfailure rat myocardial tissue.3RIPC can reduce the number of myocardial cells injury and degree of heartfailure, protect myocardial tissue. |
PDF Full Text Request