急性心肌梗死心肌黏弹性实验研究

Experimental study of myocardial viscoelasticity in mongrels with acute myocardial infarction

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(P<0.05),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(P<0.05),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(P<0.05),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(P<0.05),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(P<0.05),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(P<0.05)。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。

Objective：To study the changes of myocardial viscoelasticity and its pathological mechanism after acute myocardial infarction（AMI）in mongrels with AMI. Methods：IUIS was used to detect creep tests in six healthy mongrels before myocardial infarction（NAMI group）,at 1 hour after AMI（AMI-1 group）,and 3 hour after AMI（AMI-3 group）in diastole in vivo. Viscoelastic parameters were extracted through the three-parameter Viscoelastic model. Immunohistochemistry of microtubulin and desmin were carried out with myocardium samples. Correlation analyses were carried out in the detection results. Results：The parameters of E∞increased obviously after AMI than before AMI（P〈0.05）,they were as follows：（5.30±0.48）k Pa,（5.73±0.32）k Pa vs.（4.31±0.40）k Pa,also the parameters of E1,they were as follows：（6.78±0.41）k Pa,（11.67±0.39）k Pa vs.（5.05±0.29）k Pa. The parameters of E_2 both decreased obviously after AMI than before AMI（P〈0.05）,they were as follows：（23.07±0.28）k Pa,（10.94±0.64）k Pa vs.（29.67±0.63）k Pa,also the parameters of η,they were as follows：（0.60±0.04）Pa·s,（0.65±0.05）Pa·s vs.（0.74±0.07）Pa·s. The parameters of τ in AMI-3 group increased obviously（P〈0.05）,they were as follows：（58.91±4.52）ms vs.（23.34±0.43）ms. Desmin and microtubulin decreased obviously after AMI for 3 hours（P〈0.05）. The decrease of intracellular microtubule related with E_2、τ at 3 hours after AMI. Conclusion：Elastic hardness increases,viscous component reduces,but rely on longer relaxation and the ability of myocardial relaxation decreases in 3 hours after AMI. The decrease of diastolic capacity partly is attributed to decrease of myocardium intracellular microtubule.