本文選題：急性心肌梗死　切入點(diǎn)：蠕變?cè)囼?yàn)　出處：《重慶醫(yī)科大學(xué)學(xué)報(bào)》2016年12期 　論文類型：期刊論文

【摘要】：目的:活體檢測(cè)急性梗死后梗死心肌黏彈性的改變并探討其病理機(jī)制。方法:通過(guò)應(yīng)用介入超聲印壓檢測(cè)系統(tǒng)(intervention ultrasound indentation system,IUIS)分別在6只健康成年雜種犬梗死前、急性心肌梗死(acute myocardial infarction,AMI)后1 h、3 h用印壓法檢測(cè)舒張心肌蠕變?cè)囼?yàn),以三參量黏彈性模型提取梗死前(NAMI組)、急性心肌梗死1 h(AMI-1組)、急性心肌梗死3 h(AMI-3組)黏彈性參數(shù)。隨后對(duì)梗死心肌的微管蛋白、結(jié)蛋白進(jìn)行免疫組織化學(xué)檢測(cè),并分析其與黏彈性參數(shù)的關(guān)系。結(jié)果:AMI后1 h、3 h表征心肌硬度參數(shù)E∞較梗死前顯著增加(P0.05),分別為(5.30±0.48)k Pa、(5.73±0.32)k Pa vs.(4.31±0.40)k Pa,同樣參數(shù)E1較梗死前也明顯增加(P0.05),分別為(6.78±0.41)k Pa、(11.67±0.39)k Pa vs.(5.05±0.29)k Pa;AMI后1 h、3 h與黏性形變相關(guān)參數(shù)E_2較梗死前明顯降低(P0.05),分別為(23.07±0.28)k Pa、(10.94±0.64)k Pa vs.(29.67±0.63)k Pa,同樣參數(shù)η較梗死前也明顯降低(P0.05),分別為(0.60±0.04)Pa·s、(0.65±0.05)Pa·s vs.(0.74±0.07)Pa·s;AMI后3 h松弛時(shí)間常數(shù)τ較梗死前明顯增加(P0.05),分別為(58.91±4.52)ms vs.(23.34±0.43)ms。與梗死前比較急性心肌梗死后3 h結(jié)蛋白和微管蛋白明顯減少(P0.05)。反映舒張心肌持續(xù)形變能力參數(shù)E_2、τ與微管改變相關(guān)程度高。結(jié)論:在急性心肌梗死早期,梗死心肌硬度增加,黏性組分降低,心肌持續(xù)形變依賴更長(zhǎng)舒張期。心肌舒張能力降低原因之一是微管蛋白減少。
[Abstract]:Objective: to investigate the changes of myocardial viscoelasticity and its pathological mechanism after acute infarction in vivo. Methods: the intervention ultrasound indentation system was used to detect the myocardial viscoelasticity in 6 healthy adult mongrel dogs before infarction in vivo. The creeping test of diastolic myocardium was performed 1 h after acute myocardial infarction (AMI) and 3 h after acute myocardial infarction (AMI). Three parameter viscoelastic model was used to extract the viscoelastic parameters of NAMI group, acute myocardial infarction (AMI) group 1 h and acute myocardial infarction group 3 h AMI-3). The microtubulin and desmin of infarct myocardium were detected by immunohistochemistry. The relationship between the parameters and the viscoelastic parameters was analyzed. Results the hardness parameters E 鈭，

本文編號(hào)：1580102