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Effects Of Valsartan On No-Reflow After Myocardial Ischemia Reperfusion In Rats

Posted on:2014-10-12Degree:MasterType:Thesis
Country:ChinaCandidate:Q H MaFull Text:PDF
GTID:2254330425483351Subject:Internal Medicine
Abstract/Summary:PDF Full Text Request
ObjectiveTo evaluate the effects of valsartan on myocardial no-reflow and itsprobable mechanism in signal transduction pathway.MethodsFifty-six male SD rats were randomly assigned to four groups: shamegroup,ischemia and reperfusion group,valsartan group(valsartan10mg/kg)and valsartan+LY294002group(valsartan10mg/kg, LY2940020.3mg/kg).Allrats,except for those in shame group,received occlusion of left anteriordescending artery (LAD) for60minutes followed by120minutes ofreperfusion. Valsartan (10mg/kg) intravenous administration15minutesbefore reperfusion,and LY294002(0.3mg/kg) intravenous administration5minutes before reperfusion. Different myocardium regions of ischemia,no-reflow and infarction were recognized and assessed according to Evans bluedye,thioflavin S fluorescent dye and triphenyltetrazolium chloride (TTC)staining techniques, respectively. Serum CK-MB were detected afterexperiment.The expression of p-akt, akt, p-eNOS and eNOS was determinedby western blotting.ResultsCK-MB: Ck-mb activity increased significantly in the I/R group Comparedwith the shame group(5144.72±357.53vs983.47±185.86, P<0.01).Compared with the I/R group, valsartan reduced ck-mbactivity(2592.69±230.59vs5144.72±357.53,P<0.01), while ck-mb activity inval+LY group was higher than the val group(3985.94±213.66vs 2592.69±230.59, P<0.01);ANR and NA: Valsartan reduced the ANR from31.26%to21.60%(P<0.01), and attenuated NA from40.16%to27.93%(P<0.01), and, LY294002partially canceled the effects of valsartan(27.60±2.48vs21.60±3.29,35.90±1.76vs27.93±4.57, P<0.01).P-akt and p-eNOS: The exppression of p-akt and p-eNOS was increasedin the I/R group compared to the shame group(34.14±2.07vs29.53±3.14,20.17±2.07vs16.65±1.69, P<0.01), and Valsartan further elevated theexpression of p-akt and p-eNOS compared with the I/R group(45.00±2.76vs34.14±2.07,37.60±2.33vs20.17±2.07, P<0.01), However,LY294002decreased the expression of p-akt and p-eNOS compared with the valgroup(30.79±2.05vs45.00±2.76,24.20±2.49vs37.60±2.33, P<0.01). Theexpression of Akt, eNOS protein Among the groups had no statisticalsignificance.ConclusionValsartan can reduce the area of myocardial no-reflow afterischemia-reperfusion. This beneficial effect is partially dependant onPI3K-akt-eNOS signal transduction pathway.
Keywords/Search Tags:Ischemia Reperfusion, No-Reflow, Valsartan, Signal Transduction
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