Increased muscle sympathetic nerve activity acutely alters conduit artery shear rate patterns
Increased muscle sympathetic nerve activity acutely alters conduit artery shear rate patterns
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DOI：
10.1152/ajpheart.01133.2009
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发表时间：
2010-04-01
影响因子：
4.8
通讯作者：
Fadel, Paul J.
中科院分区：
文献类型：
--
作者：
Padilla, Jaume;Young, Colin N.;Fadel, Paul J.
首页--期刊主要分类--期刊细介绍--期刊题录与文摘--期刊详细文摘内容肌交感神经活性的增加会急剧改变导管动脉的切变率模式。Am J Physiol心脏圈Physiol 298：H1128-H1135,2010。2010年2月12日首次出版；DOI：10.1152/ajpheart.01133.2009..-越来越多的证据表明，以逆行和振荡剪应力的存在为特征的扰动流动模式诱导了致动脉粥样硬化的内皮细胞表型；然而，外围管道动脉振荡剪切曲线的机制尚不完全清楚。我们验证了这样一种假设，即肌交感神经活动(MSNA)的急性升高伴随着导管动脉逆行和振荡切变的增加。14名健康男性(25+/-1岁)进行了3种交感兴奋动作：分级下体负压(LBNP)从0到-40Torr，冷加压试验(CPT)，35%最大自主收缩握力后运动后缺血(PEI)。连续记录对侧臂的微血管造影(MSNA)、动脉血压(手指光体积描记)、肱动脉血流速度和内径(双功多普勒超声)。所有动作均使MSNA总活动量较基线显著增加(P<；0.05)。在下体负压分级过程中，逆行切变(-3.96+/-1.2基线比-8.15+/-1.8 S(-1)，-40LBNP，P<；0.05)和振荡切变指数(0.09+/-0.02基线比0.20+/-0.02任意单位，-40LBNP，P<；0.05)逐渐增大。相反，在CPT和PEI期间，MSNA和血压同时升高(P<；0.05)，逆行和振荡切变的变化很小或没有变化。这些数据表明，MSNA的急性升高与导管动脉逆行和振荡切变的增加有关，这一效应可能受到动脉血压同时升高的影响。未来的研究应该研究MSNA、动脉血压和其他潜在的剪切率模式调节因素之间的复杂相互作用。
Padilla J, Young CN, Simmons GH, Deo SH, Newcomer SC, Sullivan JP, Laughlin MH, Fadel PJ. Increased muscle sympathetic nerve activity acutely alters conduit artery shear rate patterns. Am J Physiol Heart Circ Physiol 298: H1128-H1135, 2010. First published February 12, 2010; doi: 10.1152/ajpheart.01133.2009.- Escalating evidence indicates that disturbed flow patterns, characterized by the presence of retrograde and oscillatory shear stress, induce a proatherogenic endothelial cell phenotype; however, the mechanisms underlying oscillatory shear profiles in peripheral conduit arteries are not fully understood. We tested the hypothesis that acute elevations in muscle sympathetic nerve activity (MSNA) are accompanied by increases in conduit artery retrograde and oscillatory shear. Fourteen healthy men (25 +/- 1 yr) performed three sympathoexcitatory maneuvers: graded lower body negative pressure (LBNP) from 0 to -40 Torr, cold pressor test (CPT), and 35% maximal voluntary contraction handgrip followed by postexercise ischemia (PEI). MSNA (microneurography; peroneal nerve), arterial blood pressure (finger photoplethysmography), and brachial artery velocity and diameter (duplex Doppler ultrasound) in the contralateral arm were recorded continuously. All maneuvers elicited significant increases in MSNA total activity from baseline (P < 0.05). Retrograde shear (-3.96 +/- 1.2 baseline vs. -8.15 +/- 1.8 s(-1), -40 LBNP, P < 0.05) and oscillatory shear index (0.09 +/- 0.02 baseline vs. 0.20 +/- 0.02 arbitrary units, -40 LBNP, P < 0.05) were progressively augmented during graded LBNP. In contrast, during CPT and PEI, in which MSNA and blood pressure were concomitantly increased (P < 0.05), minimal or no changes in retrograde and oscillatory shear were noted. These data suggest that acute elevations in MSNA are associated with an increase in conduit artery retrograde and oscillatory shear, an effect that may be influenced by concurrent increases in arterial blood pressure. Future studies should examine the complex interaction between MSNA, arterial blood pressure, and other potential modulatory factors of shear rate patterns.