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体内肝脏微波消融术后血管血栓形成的潜在机制

Potential Mechanisms of Vascular Thrombosis after Microwave Ablation in an in Vivo Liver.

作者信息

Chiang Jason, Nickel Kwang, Kimple Randall J, Brace Christopher L

机构信息

Department of Radiology, University of Wisconsin, 1111 Highland Ave., 1310-O, Madison, WI 53705.

Department of Radiation Oncology, University of Wisconsin, 1111 Highland Ave., 1310-O, Madison, WI 53705.

出版信息

J Vasc Interv Radiol. 2017 Jul;28(7):1053-1058. doi: 10.1016/j.jvir.2017.03.034. Epub 2017 Apr 26.

Abstract

PURPOSE

To evaluate potential biologic and thermal mechanisms of the observed differences in thrombosis rates between hepatic vessels during microwave (MW) ablation procedures.

MATERIALS AND METHODS

MW ablation antennae were placed in single liver lobes of 2 in vivo porcine liver models (n = 3 in each animal; N = 6 total) in the proximity of a large (> 5 mm) portal vein (PV) and hepatic veins (HVs). Each ablation was performed with 100 W for 5 minutes. Conventional ultrasound imaging and intravascular temperature probes were used to evaluate vessel patency and temperature changes during the ablation procedure. Vascular endothelium was harvested 1 hour after ablation and used to characterize genes and proteins associated with thrombosis in PVs and HVs.

RESULTS

Targeted PVs within the MW ablation zone exhibited thrombosis at a significantly higher rate than HVs (54.5% vs 0.0%; P = .0046). There was a negligible change in intravascular temperature in PVs and HVs during the ablation procedure (0.2°C ± 0.4 vs 0.6°C ± 0.9; P = .46). PVs exhibited significantly higher gene expression than HVs in terms of fold differences in thrombomodulin (2.9 ± 2.0; P = .0001), von Willebrand factor (vWF; 7.6 ± 1.5; P = .0001), endothelial protein C receptor (3.50 ± 0.49; P = .0011), and plasminogen activator inhibitor (1.46 ± 0.05; P = .0014). Western blot analysis showed significantly higher expression of vWF (2.32 ± 0.92; P = .031) in PVs compared with HVs.

CONCLUSIONS

Large PVs exhibit thrombosis more frequently than HVs during MW ablation procedures. Biologic differences in thrombogenicity, rather than heat transfer, between PVs and HVs may contribute to their different rates of thrombosis.

摘要

目的

评估在微波(MW)消融过程中,肝脏血管间观察到的血栓形成率差异的潜在生物学和热学机制。

材料与方法

将MW消融天线置于2个活体猪肝模型的单个肝叶中(每只动物n = 3;共N = 6),靠近一条大的(> 5 mm)门静脉(PV)和肝静脉(HV)。每次消融以100 W进行5分钟。使用传统超声成像和血管内温度探头评估消融过程中的血管通畅情况和温度变化。消融1小时后采集血管内皮,用于表征PV和HV中与血栓形成相关的基因和蛋白质。

结果

MW消融区内的目标PV血栓形成率显著高于HV(54.5%对0.0%;P = .0046)。消融过程中PV和HV的血管内温度变化可忽略不计(0.2°C ± 0.4对0.6°C ± 0.9;P = .46)。就血栓调节蛋白的倍数差异而言,PV的基因表达显著高于HV(2.9 ± 2.0;P = .0001)、血管性血友病因子(vWF;7.6 ± 1.5;P = .0001)、内皮蛋白C受体(3.50 ± 0.49;P = .0011)和纤溶酶原激活物抑制剂(1.46 ± 0.05;P = .0014)。蛋白质印迹分析显示,与HV相比,PV中vWF的表达显著更高(2.32 ± 0.92;P = .031)。

结论

在MW消融过程中,大PV比HV更频繁地出现血栓形成。PV和HV之间血栓形成倾向的生物学差异而非热传递,可能导致它们不同的血栓形成率。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34d5/5483190/afae440ed6d0/nihms864926f1a.jpg

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