| ProfaceAcute myocardial infarction ( AMI) is one of main diseases that are threatening human beings health and even lead to death. Some studies are focused on seeking for the methods of the process of left ventricular remodelling in order to reduce symptoms of AMI, improve myocardial ischaemic condition and save damgerous myocardium after AMI.Angiotensin I (2-10) is a endogenous angiotensin peptide and can be synthetized artificcially. Its pharmaceutic function is still unknown. Some studies showed that it could minimize myocardial remodeling and fibrosis. The aim of this study is to detect the effects of angiotensin I (2-10) on the expression of collagen- I ( col- I ) ^collagen-III ( col-III) and Transforming growth factor-β1 (TGF-β1) in myocardium of rats AMI. with immunnohistochemical technique. To determine if angiotensin I (2-10) affect angiogenesis after AMI and to provide a sound basis for further clinical utilization and exploiting the pharmacy of AMI.Materids and metherForty-five healthy male Wister rats (weight 200 -250g) were divided into three groups randomly, each group had fifteen rats. In experimental group and control group, the left thoractomy was performed in the fourth intercostal space,the pericardium was opend and the left coronary artery was ligated for 45 minutes, then myocardium was reperfused. All rats received angiotensin I (2-10) 50Pmol kg-1, d-1. In control group, all animals received distilled water of same dose. In sham-group, all animals were treated in same manner as previously described except that no cornary ligation was carried out. After 14 days, all animals were killed, col- I, col-III and TGF-β1 were detected with immnohistochemical technique. Computer scanned and quantitated. Software of SPSS 10 was used to examined all values.Result1. Thirty of forty-five rats surrived. Ten rats were rest in experimental group, nine rats in control group and eleven rats in sham-operated group. Total operative mortality of the surgical procedure in three groups was 33. 3% ( including early death within 24 hours) .2. Morphometric analysis with HE stain. Myocardial tissue was stained with HE and pathological changes were observed. Forty-five minutes of left coronary artery occlusion followed by reperfusion produced nontransmural myocardial infarction with sparing of a considera-le amount of subepicardion as well as a thin rim of exdocardium in the infarced zone. In experimental group and control group, infarction wasobserved, myocardial fibre was dissolved and broken and inflammatory cells infiltrated into infarction zone. Moreover, pathological changes was more serious in control group than that in experimental group. In-farct area of experimental animals was remarkally smaller than that of control animals. However, noinfarction was observed in sham-operated group, myocardial fibre arranged orderly.3. To examine the expression of col- I , col-III and TGF-β1 in myocardium with immunohistochemcal technique: The expression of col-I,col-III and TGF-β1 in myocardial cell in experimental group was lower than in culture-group ( p < 0. 001).DiscussionNowaday, there are three strategies to treat acute myocardial infarction , including chemical therapy interventional therapy and operative therapy, moreover, most emergency patients are strict to PTCA and CABG, or they can not recover the coronery bloob-flow completely after PTCA and CABG. We must find other strategy to save dying myocardium and reverse left ventricular remodelling, collagen ( col) were increased after AMI, the most of collagen are col- I, col-III. col-I, col-III may play an important role in the process of left ventricular remodelling after AMI. Transforming growth factor-β1(TGF-β1) are increased after AMI, TGF-β1 can reverse collagenase, and increase collagen remodeling.AngintensinI (2 - 10) is metabolite that angintensin I was deserted the first ammo acid-aspartic by special aminopeptidase, so it is called Des-Asp-angiotensin I. Its pharmaceutic function is unknown. It is repo...
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