| ObjectiveTo evaluate the dynamic changes of inflammatory cells and inflammatory cytokines and the relationship to the noninfarcted myocardium fibrosis after acute myocardial infarction(AMI). To explore the effects of inflammation in noninfarcted myocardium fibrosis and the effects of allopurinol on them.MethodsExperimental myocardial infarction was created by left coronary artery ligation in rats. After 24 hours of the above procedure, surviving rats were randomly assigned to the following 2 groups : (1) AMI control group(n=58); (2) Allopurinol treatment group(n=58). the other randomly selected rats were sham-operated group(n=34). Then the rats in these three groups were redivided into five subgroups according to the course of intervention:2d,4d,7d,14d and 28d subgroups. By the end of each course the rats were killed, the mortality of all rats was calculated and hemodynamics index of rats were measured before rats being sacrificed, the wet-to-dry ratio of the lungs was measured . Morphological characteristics were evaluated with HE, Sirus-red; the size of infarction and collagen volume fraction (CVF) of non-infarction myocardium were assessed or calculated respectively with compute-assisted image analysis system (Image-Pro Plus, Version: 4.5).Mast cells in the noninfarcted region were identified with toluidine blue staining and tryptase immunohistochemistry staining. Macrophages were demonstrated with ED1 immunohistochemistry staining. Immunohistochemistry staining was performed to lable interleukin-6 (IL-6), monocyte chemoattractant protein-1(MCP-1) and nuclear factor kappa B(NF-κB) in the noninfarcted region. The IL-6 and MCP-1 were extracted and measured by western blot analysis.Correlation analysis was used to analyse the relationship of inflammatory cells and cytokines to CVF and LVEDP respectively.
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