急性心肌梗死心肌黏弹性实验研究

发布时间：2018-03-07 16:42

  本文选题：急性心肌梗死　切入点：蠕变试验　出处：《重庆医科大学学报》2016年12期 　论文类型：期刊论文

【摘要】：目的:活体检测急性梗死后梗死心肌黏弹性的改变并探讨其病理机制。方法:通过应用介入超声印压检测系统(intervention ultrasound indentation system,IUIS)分别在6只健康成年杂种犬梗死前、急性心肌梗死(acute myocardial infarction,AMI)后1 h、3 h用印压法检测舒张心肌蠕变试验,以三参量黏弹性模型提取梗死前(NAMI组)、急性心肌梗死1 h(AMI-1组)、急性心肌梗死3 h(AMI-3组)黏弹性参数。随后对梗死心肌的微管蛋白、结蛋白进行免疫组织化学检测,并分析其与黏弹性参数的关系。结果:AMI后1 h、3 h表征心肌硬度参数E∞较梗死前显著增加(P0.05),分别为(5.30±0.48)k Pa、(5.73±0.32)k Pa vs.(4.31±0.40)k Pa,同样参数E1较梗死前也明显增加(P0.05),分别为(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与黏性形变相关参数E_2较梗死前明显降低(P0.05),分别为(23.07±0.28)k Pa、(10.94±0.64)k Pa vs.(29.67±0.63)k Pa,同样参数η较梗死前也明显降低(P0.05),分别为(0.60±0.04)Pa·s、(0.65±0.05)Pa·s vs.(0.74±0.07)Pa·s;AMI后3 h松弛时间常数τ较梗死前明显增加(P0.05),分别为(58.91±4.52)ms vs.(23.34±0.43)ms。与梗死前比较急性心肌梗死后3 h结蛋白和微管蛋白明显减少(P0.05)。反映舒张心肌持续形变能力参数E_2、τ与微管改变相关程度高。结论:在急性心肌梗死早期,梗死心肌硬度增加,黏性组分降低,心肌持续形变依赖更长舒张期。心肌舒张能力降低原因之一是微管蛋白减少。
[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，

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