| Backgroud：Acute myocardial infarction (AMI) is a common type of coronaryheart disease，is also the number one killer threating humans’ lives,In the past,AMIhas the higher incidence in the elderly,but according to the recent clinical studies,ithas a trend of that myocardial infarction population is moving to the younger,evenconcluding thirty-four-year-old young adults(as the pressure of life，the fast pace oflife，irregular diet).In2011,relevant survey data shows that ACS incidence rate inpeople under the age of40years has reached100/1000000,and the above figuresshould make us wake-up,it has become an urgent matter to prevent and treat the AMI.AMI, is one of the most dangerous kinds of disease in all emergency patientsadmitted by hospital,For a long time, through the explore and study,the spect ofdiagnosis and treatment technologies has been improved and widespread.Such asdiagnosed,related medicine and intervene treat all have made a great progress,but there-ischemia and high mortality rates remain burning question we need to solve asquick as we can.So pay more attention to the analyze of the disease causing theoryand clinical manifestations plays the same important roles as the introduce newdiagnosed methods and new treatment medicine use in improving clinical patientsoutcomes.The basic principle of AMI treatment is as early as possible to save the dyingmyocardial improve myocardial blood supply to restore effective blood flow,protectand preserve the function of the heart,to narrow the scope of myocardial infarction,timely processing of a variety of serious complications,prevent sudden death,cardiacinterventional techniques (PCI) is the primary means for the treatment of AMI, butthe right choice for clinical drug also can not be ignored,the early application ofeffective drugs,the prognosis of AMI and reduce the mortality rate of recurrence of a significant role.This paper mainly studies the protective effect of recombinant humanbrain natriuretic peptide on myocardial ischemia in AMI.Objective: To observe the protective effect of recombinant human brainnatriuretic peptide(rhBNP) on acute myocardial ischemia in rats.Methods: We may divided30Wistar rats (all females) into three groupsrandomly,each group is10,and then by ligation of the left anterior descendingcoronary artery of each group rats to preparation of acute myocardial ischemiamodel,sham group:the group only wear lines but not ligate the left coronaryarteryanterior descending artery,after that give saline0.5ml/100g by sublingualintravenous immediately;model group:In accordance with the method of preparationof ischemia model in rats,ligation of the left anterior descending coronary artery,afterligate and give saline0.5ml/100g by sublingual vein immediately;rhBNP group:thegroup use the same ligation method with the model group,sublingual intravenousrhBNP0.15μg/100g immediately after ligation,and the injection volume is0.5ml/100g.Then observe each group’s ECG changes,Through the abdominal aorticBod collection after two hours,with the Microplate reader analysis detected theactivities of serum CK,AST and LDH,while application in charge photometer(Colorimetric) to measure the activity of SOD and the content of MDA,recordingvarious data,then remove the rat heart and rinse cardiac hemorrhage with saline,removing the atrial tissue,the right ventricle and fat, and put the left ventricular slicesinto the TTC phosphate buffer at37℃constant temperature water bath about15min,then remove them to fix in100ml/L formalin solution,visual observation ofmyocardial infarction area,observe myocardial infarct size and calculate themyocardial infarct size,after TTC staining,lsat with digital camera to take pictures,while sacrificing the rat left ventricular tissue of each group,make the myocardialslice with the thickness is about2mm,put them in10%formalin solution to fix,conventional HE staining,observe myocardial pathological changes with lightmicroscope. Results:1. After string the Sham group’s ECG may appear transient ST-Tchanges,and then returned to normal electrocardiogram;after ligate the left anteriordescending artery the model group appear ST segment elevation (≥0.1mv)immediately,then with high angle Twave fused into a banner-like changes, in rhBNPgroup after ligate LDA ST-segment elevation (≥0.1mv),after give rhBNP STsegment may down to the baseline near;2.Compared with sham-operated rats, themodel serum CK,LDH and AST were significantly increased (P <0.05or P <0.01) ascompared with the model group,the rhBNP group the CK,LDH and AST’s activity inserum was significantly lower (P <0.05or P <0.01);3.Compared with the shamgroup, model group the MDA’s content in serum was significantly increased (P<0.01),SOD’s activity was significantly decreased (P <0.01),compared with themodel group rats,the rhBNP group MDA’s content significantly decreased (P<0.05),SOD’s activity was significantly increased (P <0.05);4.There is no significantdifference in three groups of left ventricular mass,compared with the sham group,themodel rats’s myocardial infarction weight and infarct size was significantly higher (P<0.01); compared with the model group, the rhBNP group rats’s myocardialinfarction weight is reduced, and the infarction of range is reduced (P <0.01),5.TTCstaining: by eye view of the deep staining of the sham-operated group (brick red),noobvious white areas,the model group showed obvious white areas-the infarcted area,the white area of rhBNP group compared with the model group significantlyreduced,show that infarction narrow;6.There is no significant changes aboutmyocardial morphology in sham group,and model group cardiomyocyte hypertrophymyocardial karyopyknosis,diffuse vacuolar degeneration of myocardial cells,myocardial interstitial fibrosis and disarranged structure and cell disorder,blurredlocal stripes not clear or disappeared,partly myocardial necrosis and inflammatorycell infiltration and capillary bleeding,the rhBNP group also appear pathologicalchanges of myocardial injury but the extent lesser than model group.Conclusions:1.rhBNP can improve heart damage caused by myocardialischemia and myocardial blood supply;2.rhBNP can reduce myocardial infarct size, play a role in myocardial protection;3.rhBNP can reduce MDA content,increasedSOD activity,reduce the production of free radicals in the ischemic myocardium, toenhance myocardial cells antioxidant capacity,reducing myocardial oxygenconsumption,reduction of myocardial cellsinjury,which play the role of myocardialprotection. |
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