Effects of aging and coronary artery disease on sympathetic neural recruitment strategies during end-inspiratory and end-expiratory apnea
Effects of aging and coronary artery disease on sympathetic neural recruitment strategies during end-inspiratory and end-expiratory apnea
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DOI：
10.1152/ajpheart.00334.2016
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发表时间：
2016-10-01
影响因子：
4.8
通讯作者：
Shoemaker, J. Kevin
中科院分区：
文献类型：
--
作者：
Badrov, Mark B.;Lalande, Sophie;Shoemaker, J. Kevin
作为对急性生理应激的反应，交感神经系统通过增加低阈轴突的放电频率、募集高阈轴突的潜在亚群和/或突触延迟的急性改变来改变神经流出。衰老和冠状动脉疾病（CAD）经常改变传出肌交感神经活动（MSNA）。因此，我们研究了CAD （n = 14； 61 +/- 10年）和/或健康老龄化而没有CAD （OH; n = 14； 59 +/- 9年）是否改变了通常在年轻健康个体（YH; n = 14； 25 +/- 3年）中观察到的这些招募策略。在基线和最大自主吸气末（EI）和呼气末（EE）呼吸期间测量MSNA（微神经造影）。采用一种新的动作电位分析技术对动作电位模式进行了研究。在EI-和ee -呼吸暂停期间，各组AP频率均升高（均P < 0.05）。在EI-和EE-呼吸暂停期间，YH （EI: δ 6 +/- 4 APs/ burst, EE: δ 10 +/- 6 APs/ burst， P均< 0.01）和OH （EI: δ 3 +/- 3 APs/ burst, EE: δ 4 +/- 5 APs/ burst， P均< 0.01）和CAD （EI: δ 1 +/- 3 APs/ burst, EE: δ 2 +/- 3 APs/ burst， P均= NS）中，每次综合发作的平均AP含量增加。将ap按峰间振幅归类为“簇”时，YH患者EI-和EE-呼吸暂停期间总簇数增加（EI: δ 5 +/- 2; EE: δ 6 +/- 4；均P < 0.01）， EI-呼吸暂停期间仅OH患者（EI: δ 1 +/- 2; P < 0.01; EE: δ 1 +/- 2; P = NS）， CAD患者（EI: δ -2 +/- 2; EE: δ -1 +/- 2；均P = NS）。在所有组中，EI-和ee -呼吸暂停期间，AP集群大小-潜伏期曲线在每个相应集群中向下移动（均P < 0.01）。因此，固有的失调存在于衰老和CAD中呼吸暂停相关交感神经流出的中心特征中。
In response to acute physiological stress, the sympathetic nervous system modifies neural outflow through increased firing frequency of lower-threshold axons, recruitment of latent subpopulations of higher-threshold axons, and/or acute modifications of synaptic delays. Aging and coronary artery disease (CAD) often modify efferent muscle sympathetic nerve activity (MSNA). Therefore, we investigated whether CAD (n = 14; 61 +/- 10 yr) and/or healthy aging without CAD (OH; n = 14; 59 +/- 9 yr) modified these recruitment strategies that normally are observed in young healthy (YH; n = 14; 25 +/- 3 yr) individuals. MSNA (microneurography) was measured at baseline and during maximal voluntary end-inspiratory (EI) and end-expiratory (EE) apneas. Action potential (AP) patterns were studied using a novel AP analysis technique. AP frequency increased in all groups during both EI- and EE-apnea (all P < 0.05). The mean AP content per integrated burst increased during EI- and EE-apnea in YH (EI: Delta 6 +/- 4 APs/ burst; EE: Delta 10 +/- 6 APs/ burst; both P < 0.01) and OH (EI: Delta 3 +/- 3 APs/ burst; EE: Delta 4 +/- 5 APs/ burst; both P < 0.01), but not in CAD (EI: Delta 1 +/- 3 APs/ burst; EE: Delta 2 +/- 3 APs/ burst; both P = NS). When APs were binned into "clusters" according to peak-to-peak amplitude, total clusters increased during EI- and EE-apnea in YH (EI: Delta 5 +/- 2; EE: Delta 6 +/- 4; both P < 0.01), during EI-apnea only in OH (EI: Delta 1 +/- 2; P < 0.01; EE: Delta 1 +/- 2; P = NS), and neither apnea in CAD (EI: Delta -2 +/- 2; EE: Delta -1 +/- 2; both P = NS). In all groups, the AP cluster size-latency profile was shifted downwards for every corresponding cluster during EI- and EE-apnea (all P < 0.01). As such, inherent dysregulation exists within the central features of apnea-related sympathetic outflow in aging and CAD.