Atrial fibrillation pacing decreases intravascular shear stress in a New Zealand white rabbit model: implications in endothelial function.

Atrial fibrillation pacing decreases intravascular shear stress in a New Zealand white rabbit model: implications in endothelial function.
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心房颤动起搏降低新西兰白兔模型中的血管内剪切应力:对内皮功能的影响。

DOI:
10.1007/s10237-012-0437-0
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发表时间:
2013
影响因子:
3.5
通讯作者:
Hsiai,TzungK
Hsiai,TzungK
中科院分区:
工程技术2区
文献类型:
--
作者:
Jen,Nelson;Yu,Fei;Lee,Juhyun;Wasmund,Steve;Dai,Xiaohu;Chen,Christina;Chawareeyawong,Pai;Yang,Yongmo;Li,Rongsong;Hamdan,MohamedH;Hsiai,TzungK

文献摘要

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心房颤动(房颤)的特征是多个快速不规则的心房除极,导致快速的心室反应超过100次/分钟(Bpm)。我们假设快速和不规则起搏降低了血管内切应力(ISS),这意味着调节血管内皮细胞反应。为模拟房颤,我们对新西兰大白兔(n=4)的左心耳进行快速和不规则的起搏。记录房性和室性节律的体表心电图,用低温传感器测量血管内对流换热,由此推断ISS。快速和不规则起搏降低了动脉收缩和舒张压(基线,99/75毫米汞;快速规则起搏,92/73;快速不规则起搏,90/68;P<0.001,n=4),时间梯度(从1,275±80降至1,056±180达因/厘米~2),以及ISS降低(从基线的32.0±2.4降至22.7±3.5达因/厘米2)。计算流体力学程序表明,在给定的导管与血管直径比、剪切应力范围和导管位置下,实验推断的ISS提供了与计算的壁切应力非常接近的结果。在保持时间平均切应力的体外流动系统中,我们进一步证明了150bpm的快速脉搏频率下调了内皮细胞一氧化氮,促进了超氧化物歧化酶(O2.−)的产生,并增加了单核细胞与内皮细胞的结合。这些发现表明,快速起搏减少了ISS和,而快速脉搏调节内皮反应。
Atrial fibrillation (AF) is characterized by multiple rapid and irregular atrial depolarization, leading to rapid ventricular responses exceeding 100 beats per minute (bpm). We hypothesized that rapid and irregular pacing reduced intravascular shear stress (ISS) with implication to modulating endothelial responses. To simulate AF, we paced the left atrial appendage of New Zealand White rabbits (n= 4) at rapid and irregular intervals. Surface electrical cardiograms were recorded for atrial and ventricular rhythm, and intravascular convective heat transfer was measured by microthermal sensors, from which ISS was inferred. Rapid and irregular pacing decreased arterial systolic and diastolic pressures (baseline, 99/75 mmHg; rapid regular pacing, 92/73; rapid irregular pacing, 90/68;p< 0.001,n= 4), temporal gradients (from 1,275 ± 80 to 1,056 ± 180 dyne/cm2s), and reduced ISS (from baseline at 32.0 ± 2.4 to 22.7 ± 3.5 dyne/cm2). Computational fluid dynamics code demonstrated that experimentally inferred ISS provided a close approximation to the computed wall shear stress at a given catheter to vessel diameter ratio, shear stress range, and catheter position. In an in vitro flow system in which time-averaged shear stress was maintained at, we further demonstrated that rapid pulse rates at 150 bpm down-regulated endothelial nitric oxide, promoted superoxide (O2.−) production, and increased monocyte binding to endothelial cells. These findings suggest that rapid pacing reduces ISS and, and rapid pulse rates modulate endothelial responses.