首页> 外文期刊>Autonomic neuroscience: basic & clinical >Myogenic activity in autoregulation during low frequency oscillations.
【24h】

Myogenic activity in autoregulation during low frequency oscillations.

机译:低频振荡期间自我调节的肌源性活动。

获取原文
获取原文并翻译 | 示例
           

摘要

Lower body negative pressure (LBNP) was applied in eight human subjects to trigger low frequency oscillations in order to study the nature of functional coupling between the hemodynamic and autonomic nervous systems, with particular focus on how the myogenic response fits within this coupling. To this end muscle sympathetic nerve activity (MSNA), mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were measured at baseline and during LBNP and were then examined in both the time and frequency domains. At the height of low frequency oscillations (~0.1Hz) there was a strong coupling between all the five indices, marked by perfect alignment of their oscillatory frequencies. Results in the time domain show that a fall in MAP is followed by a fall in TPR at 1.58s SD 0.69), a rise in heart rate at 2.64s (SD 0.98), a rise in cardiac output at 3.72s (SD 0.60), a peak in MSNA at 5.71s (SD 1.27) and, finally, a rise in TPR at 7.13s (SD 1.02). A possible interpretation of the latter is that a drop in MAP first triggers a drop in TPR via a myogenic response before the expected rise in TPR via a rise in MSNA. In other words, following a drop in arterial pressure, myogenic response controls vessel diameter before this control is taken over by MSNA. These findings provide a possible resolution of a longstanding conceptual argument against attributing a significant role for the myogenic response in blood flow autoregulation.
机译:为了研究血液动力学和自主神经系统之间功能性偶联的性质,在八名人类受试者中应用了较低的身体负压(LBNP)来触发低频振荡,尤其着重于肌源性反应如何适应这种偶联。为此,在基线和LBNP期间测量了肌肉交感神经活性(MSNA),平均动脉压(MAP),心率(HR),心输出量(CO)和总外周阻力(TPR),然后在这两个阶段进行了检查时域和频域。在低频振荡的高度(〜0.1Hz),所有五个指标之间都存在强耦合,其振荡频率完美对齐。时域结果显示,MAP下降,TPR在1.58s SD 0.69下降,心率在2.64s(SD 0.98)上升,心排血在3.72s(SD 0.60)上升。 ,则MSNA在5.71s(SD 1.27)达到峰值,最后,TPR在7.13s(SD 1.02)上升。后者的一种可能解释是,MAP的下降首先通过成肌反应触发TPR的下降,然后再通过MSNA的上升来预期TPR的上升。换句话说,在动脉压下降之后,肌原性反应可控制血管直径,然后再由MSNA进行控制。这些发现提供了一个长期的概念性论据的可能解决方案,该论据反对将肌源性反应归因于血流自动调节中的重要作用。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号