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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 detect the changes of myocardial viscoelasticity after acute infarction and to explore its pathological mechanism. Methods: The diastolic pressure was measured by using the invasive ultrasound before application of intervention ultrasound indentation system (IUIS) in 6 healthy adult mongrel dogs, 1 h and 3 h after acute myocardial infarction (AMI) Myocardial creep test, the viscoelastic parameters of AMI-3 group were collected before infarction (NAMI group), AMI-1 group and AMI-3 group by three-parameter viscoelastic model. Subsequently, the expression of tubulin and desmin in infarcted myocardium were detected by immunohistochemistry, and the relationship between them and viscoelastic parameters was analyzed. Results: The parameters of myocardial stiffness at 1 h and 3 h after AMI were significantly higher (P <0.05) than that before infarction (5.30 ± 0.48 kPa, 5.73 ± 0.32 kPa vs. 4.31 ± 0.40 respectively) (P <0.05), the same parameter E1 was significantly higher than before infarction (P <0.05), respectively, 6.78 ± 0.41 kPa, 11.67 ± 0.39 kPa vs. 5.05 ± 0.29 kPa; 1 h after AMI, 3 h and viscosity related parameters E 2 were significantly lower than those before infarction (P <0.05), respectively, (23.07 ± 0.28) kPa, (10.94 ± 0.64) kPa vs. (29.67 ± 0.63) k Pa, (0.60 ± 0.04) Pa · s, (0.65 ± 0.05) Pa · s vs. (0.74 ± 0.07) Pa · s, respectively, compared with those before infarction (P <0.05). The relaxation time constant τ Which was significantly higher than that before infarction (P <0.05), respectively (58.91 ± 4.52) ms vs. (23.34 ± 0.43) ms. Compared with pre-infarction acute myocardial infarction 3 h after desmin protein and tubulin were significantly reduced (P <0.05). The parameter E_2, τ that reflects the sustained deformation of diastolic myocardium has a high correlation with microtubule changes. Conclusion: In the early stage of acute myocardial infarction, myocardial infarction increased, viscosity decreased, and sustained myocardial deformation depended on longer diastolic phase. One of the reasons for the decrease of myocardial diastolic capacity is the decrease of tubulin.