| Background and objectivesThe incidence of acute myocardial infarction (AMI) was increased year by year,and this way has influenced people’s survival in the current worldwide. becomeincreasingly the focus of people.The inflammatory reaction and the ventricularremodeling after acute myocardial infarction has affected the ventricular systolicfunction, the prognosis of patients and long-term survival rate seriously.After acute myocardial infarction has a series of changes in myocardial cells,such as neutrophils seepage; myocyte hypertrophy, apoptosis, embryonic genesregeneration; the changing of myocardial extracellular matrix quality andcomposition;the increasing of myocardia quality and ventricular volume, thechanging of of ventricular shape. Neutrophils seepage and the changing of myocardialquality causing ventricular remodeling is of great significance to the prognosis ofmyocardial infarction. If there is a gene can alleviate a series of change. The reducedmortality of mortality of myocardial infarction can protect the heart. Bradykin widelyexists in many tissues and organs to participate in a variety of physiological andpathological processes such as cardiovascular, nervous system and kidney function.Bradykin has a important role to the changing of myocardial cells after myocardial infarction.The paper mainly discusses the mechanism of B1receptor to reduce themyocardial remldelingafter myocardial infarction such as vasodilatation,inflammatory response, tissue reconstruction.The paper also discusses enalaprilat andchlorine can increa the express of B1receptor. As temple enalaprilat and losartanprevention and treatment of ventricular remodeling after acute myocardial infarctionprovide important theoretical basis.Methods1.60pcs healthy male mature SD rats with the weight220-270g/pc and the age10weeks old respectively.Rats were randomly divided into sham operation group(SH)acute myocardial infarction group (AMI) and pravastatin group (P). Myocardialinfarction group extractioning myocardial infarction organization on6h,24h3w, isdivided into6hMI group24hMI group and3w groups(each group10) Pravastatingroup were divided into three weeks enalapril group (A)，three weeks losartan group(B).2.10%Chloral hydrate were injected into abdomen to anesthetize the ratswhich had been weighed. Under the condition of respirator, ligated the left coronaryartery to induce the acute myocardial infarction model of rats. Group A was treatedwith enalapril solution (2.5mg/kg/d) in the time point of the same, group B was givenlosartan solution (80mg/kg/d) in the time point of the same.Distilled water weregavied to the other4groups in the same amount of time every day.3. After hematoxylin-eosin(HE) staining,samples through the olympus opticalmicroscope were carefully observed on the morphological changes of thesemyocardial cells.4.The expression of BDKB1R protein and mRNA were detected byimmunohistochemistry and RT-PCR respectively.The relative expression BDKB1Rprotein and mRNA in the six groups were analysed by one-way ANOVA an usingsSSPS oftware package.5. Analyse the data by exploiting SSPS17.0. All the quantitative data werepresented as x±s. Multiple comparisons were completed by using the one way analysis of variance (ANOVA) and the sattistical significance of differences betweenthe two groups was assessed with the least-significant difference(LSD) test. Sattisticalsignificance was set at α=0.05.Results1.The morphological changes of myocardial tissues The myocardial cell ingroup SH ranged in order,without myocardial infarction,inflammatory cellinfiltration and fibrosis of stroma cells. The myocardial cell in group AMI happenednecrosis, with inflammatory cells infiltration, hyperplasia of collagen fibers. Themyocardial cell in the infarction area happened myocyte hypertrophy, disorderedarrangement, interstitial collagen hyperplasia. The myocardial cell in group Pcompared with the group AMI, myocyte hypertrophy, inflammatory cells infiltration,interstitial fibrosis reduce significantly and the myocardial cell rangrd in order.2. Almost no protein and mRNA of BDKB1R express in the group SH. In6hMI,24h MI group,3W MI group, group A and group B the BDKB1R expressionincreased (P <0.05).6h MI group compared with24h MI group the BDKB1Rexpression decreased (P <0.05).3W group compares with6h MI the expressdecreased (P <0.05).3W group decreased compared with group A (P <0.05).3weeks group reduced in the B group (P <0.05). In group A the express increase rthan the group B (P <0.05).conclusions1. The expression of BDKB1R increases after myocardial infarction and theexpress began to increasein6h maximum24h,3w declineing gradually.2. Enalapril and losartan may regulate the express of BDKB1R and decrease，which may be one of the mechanisms to protect myocardial after AMI.. |
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