| Objective：The main purpose of this experiment is to observethe effects of different dosages of bisoprolol on blood NO and vascularMMP9, VEGF expression in atherosclerosis rats. Methods:1. fiftysix-weeks-old wister rats (weight180±40g) distribute into five groupsrandonmly:(1)Group A(Blank control):to breed with ecumenic feed;(2)Group B(Atherosclerosis group):to breed with superlipoidfeed(include80.3%ecumenic feed,2%cholesterol,0.5%sodiumcholate,0.2%propylthiouracil,10%lard,7%white sugar),and to injectvitamin D which volume dose is600thousand u/kg in three days inperitoneal cavity at least every30days.(3)Group C(Bisoprololintervention group1):to breed with superlipoid feed,and to inject vitaminD which volume dose is600thousand u/kg in three days in peritonealcavity at least every30days, and to intragastric administration withbisoprolol which dose is1.25mg/kg/d per one rat.(4)GroupD(Bisoprololintervention group2):to breed with superlipoid feed,and to inject vitaminD which volume dose is600thousand u/kg in three days in peritonealcavity at least every30days, and to intragastric administration withbisoprolol which dose is2.5mg/kg/d per one rat.(5)Group E(Bisoprololintervention group3):to breed with superlipoid feed,and to inject vitaminD which volume dose is600thousand u/kg in three days in peritoneal cavity at least every30days, and to intragastric administration withbisoprolol which dose is5.0mg/kg/d per one rat.2.After13weeks,4mlblood was extracted from chambers of heart of alive rat, injected into apipe with0.5%sodium citrate,detected the content of NO and NOS afterbeing centrifugated on2000r/min.3. The aorta of rat was separated fromthe opening to where the descending aorta has the first arborization,andseparated into two pieces from the boundaries of arcus aorta and aortaThoracica. In order to aortic arch segment for paraffin embedding fixing,do HE staining after Paraffin slicing into4um and immunohistochemistryof MMP9and VEGF.4. Statistical method:The results were showed bymeans plus or subtracting standard, observed thehomoscedasticity,ONE-WAY AONVA, the deviation of between groupsmeans we compared by LSD.The software SPSS17.0for windows wasused to analyze the data. Results:1. in pathological sections we sawthat:group A:Arterial intimal smooth and complete, each layer of clearstructure, no foam cells;group B:Surface visible fiber hat, fiber surfaceproliferative disorders, tube wall to lumen is remarkable, the visibleamount of foam cell formation, deep visible some lipid deposition;groupC:Wall surface is still visible fibrous cap and to highlight the bureaucratic,number of visible foam cells and lipid and necrotic material deposition,endothelial integrity;group D:The surface of thin fibrous cap, the tubewall to lumen highlight is not obvious, the visible foam cells and lipid;group E:Compared with group D, reduced significantly, visibleendothelial slightly incomplete and a small amount of foam cells.2.SerumNO content:group A:31.656±5.158,group B:8.608±2.294,groupC:10.032±2.133,group D:15.988±2.393,group E:23.314±4.274. B groupcompared with A group P <0.05, C group and B group showed nosignificant difference, P>0.05, D group and E group compared with Bgroup, P <0.05, D group and E group compared with statisticalsignificance P <0.05.3.Serum NOS content:group A:17.994±0.842,groupB:10.263±1.306,group C:10.689±1.387,group D:13.464±0.921,groupE:16.105±0.946. B group compared with A group P <0.05, C group andB group showed no significant difference, P>0.05, D group and E groupcompared with B group, P <0.05, D group and E group compared withstatistical significance P <0.05.4.Each group of vascular VEGF averageoptical density:group A:14.526±4.725,group B:167.699±25.745,groupC:161.708±30.081,group D:100.777±19.453,group E:56.857±27.685. Bgroup compared with A group P <0.05, C group and B group showed nosignificant difference, P>0.05, D group and E group compared with Bgroup, P <0.05, D group and E group compared with statisticalsignificance P <0.05.5.Each group of vascular MMP9average opticaldensity:group A:11.936±5.045,group B:137.577±32.548,groupC:123.562±27.071,group D:83.691±20.233,group E:46.510±18.087. Bgroup compared with A group P <0.05, C group and B group showed no significant difference, P>0.05, D group and E group compared with Bgroup, P <0.05, D group and E group compared with statisticalsignificance P <0.05.Conclusion:1.The model of Atherosclerosis can becopied successfully by breeding superlipoid feed and injecting vitaminD.2.The level of blood NO and NOS was apparently reduced inatherosclerosis rat. it was explained that endothelial dysfunction was onemechanism in the formation of atherosclerosis.3.the expression of MMP9was apparently raised in the tissues of atherosclerosis, it was explainedthat extracellular matrix degradation was one mechanism in theformation of atherosclerosis and unstable plaque.4. the expression ofVEGF was apparently raised in the tissues of atherosclerosis, it wasexplained that vascular endothelial excessive proliferation was onemechanism in the formation of atherosclerosis.5.after bisoprololintervene, blood NO and NOS was apparently raised，and the expressionof vascular MMP9, VEGF was apparently reduced after bisoprololintervened, it was explained bisoprolol can bring into play resistatherosclerosis via ameliorate endothelial function, prevent endotheliumhyperplasia and reduce the extracellular matrix degradation. |
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