Echocardiography allows for analysis of pulmonary arterial flow in mice with congenital diaphragmatic hernia.

Echocardiography allows for analysis of pulmonary arterial flow in mice with congenital diaphragmatic hernia.
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DOI:
10.1016/j.jss.2017.06.080
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发表时间:
2018-01
期刊:
The Journal of surgical research
影响因子:
--
通讯作者:
McLean SE
McLean SE
中科院分区:
其他
文献类型:
--
作者:
Shah M;Phillips MR;Quintana M;Stupp G;McLean SE

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先天性膈疝(CDH)是一种与肺发育不全和肺动脉高压(PAH)相关的结构性出生缺陷。我们假设超声心动图提供了一种评估实时右心室 (RV) 功能、重构和肺动脉 (PA) 血流的方法。对 2-3 个月龄的 Slit3 野生型 (WT) (n = 6) 和敲除 (KO) (n = 5) 小鼠进行分析。使用异氟烷麻醉小鼠。进行超声心动图分析左心室和右心室壁厚度、内径 (ID) 和功能。使用彩色多普勒分析 PA 和三尖瓣的血流。与 WT 小鼠相比,KO 小鼠有显着的 RV 扩张,平均 RVID 分别为 1.99 mm 和 1.26 mm(P = 0.007)。与 WT 相比,KO 小鼠 PA 中的血流发生了改变,PA 速度时间指数升高,分别为 30.68 mm 与 22.13 mm(P = 0.012),PA 峰值速度升高,分别为 952.61 mm/s 与 628.73 mm/s(P = 0.003),肺加速时间减少,分别为 8.94 ms 与 16.18 ms(P = 0.002),分别。通过测量三尖瓣反流峰值速度和右心室流出道速度时间指数计算得出的肺血管阻力,KO 小鼠与 WT 小鼠相比有所增加,分别为 17.61 mm2/s 和 8.91 mm2/s (P = 0.003)。患有 CDH 的 Slit3 KO 小鼠显示出 PAH 和由此导致的 RV 扩张的证据。通过直接心脏穿刺,KO 小鼠中右心室收缩压升高已被证明是 PAH 的证据。超声心动图可以直接分析 PA 和实时 RV 功能,而无需牺牲鼠标。这种评估模式允许对患有 PAH 和 CDH 的小鼠进行纵向研究。
Congenital diaphragmatic hernia (CDH) is a structural birth defect associated with pulmonary hypoplasia and pulmonary arterial hypertension (PAH). We hypothesize that echocardiography provides a method to assess real-time right ventricle (RV) function, remodeling, and pulmonary artery (PA) flow. Slit3 wild-type (WT) (n = 6) and knockout (KO) (n = 5) mice were analyzed at 2–3 months of age. Mice were anesthetized using isoflurane. Echocardiography was performed to analyze left and right ventricular wall thickness, internal diameter (ID), and function. Color Doppler was used to analyze flow in the PA and across the tricuspid valve. There was significant RV dilation in the KO mice versus WT, with an average RVID of 1.99 mm versus 1.26 mm, respectively (P = 0.007). Flow in the PA of KO mice was altered compared to WT, with elevated PA velocity time indices, 30.68 mm versus 22.13 mm (P = 0.012), elevated PA peak velocities, 952.61 mm/s versus 628.73 mm/s (P = 0.003), and decreased pulmonary acceleration times, 8.94 ms versus 16.18 ms (P = 0.002), respectively. Pulmonary vascular resistance, calculated by measuring tricuspid regurgitation peak velocity and right ventricular outflow tract velocity time index, was increased in KO versus WT mice, 17.61 mm2/s versus 8.91 mm2/s (P = 0.003), respectively. Slit3 KO mice with CDH show evidence of PAH and resultant RV dilation. Using direct cardiac puncture, elevated RV systolic pressures have been demonstrated in KO mice as evidence of PAH. Echocardiography allows direct analysis of the PA and real-time RV function without sacrifice of the mouse. This mode of evaluation allows longitudinal study in mice with PAH and CDH.
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