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Modeling autonomic peripheral vascular control.

机译：模拟自主神经末梢血管控制。

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摘要

The regulation of peripheral vascular resistance (RPV) is believed to be largely sympathetically-mediated. Thus assessment of R PV control would allow us to infer valuable information regarding sympathetic nervous activity. Variability in RPV is generally attributed to the baroreflex control of total peripheral resistance (TPR). Although it is known that respiration affects sympathetic outflow and deep breaths, akin to sighs, can lead to peripheral vasoconstriction, the respiratory modulation of TPR has been little studied. In the present study, we utilized noninvasive surrogate measures of RPV to examine the two mechanisms that influence its variability: the baroreflex control of peripheral vascular resistance and the respiratory-peripheral vascular resistance coupling. The first surrogate measure was obtained from peripheral arterial tonometry (PAT). PAT measured the changes in volume at the finger tip, reflecting the vasoconstriction response as the reduction in its signal amplitude. The other surrogate measure was obtained from laser Doppler flowmetry, which monitors microvascular perfusion. The results of this study suggest that RPV fluctuations were directly modulated by respiration rather than through indirect effect of respiratory modulation of arterial blood pressure (ABP). The simulation model developed based on previous literatures pertinent to short-term blood pressure regulation could not reproduce the sigh-vasoconstriction response as observed in the experimental data. The minimal modeling approach was employed to estimate this respiratory coupling effect, which would be incorporated into the simulation model. By means of both modeling approaches, we demonstrated that only after the direct respiratory modulation mechanism was added to the simulation model that a similar vasoconstriction response following a sigh could be reproduced.;The linear and nonlinear dynamics as well as the interaction effect involved in the modulation of RPV through changes in ABP and respiration were investigated in obese pediatric subjects exposed to orthostatic stress and subjects with sickle cell disease before and after blood transfusion treatment. In the obese pediatric subject group, we found that the linear gains of both the TPR baroreflex as well as the respiratory coupling mechanisms diminished as a result of orthostatic stress. The reduction in these gains suggests that sympathetic modulation of TPR decreased in spite of a rise in sympathetic tone. Orthostatic stress was found to lead also to a reduction in the strength of the nonlinear behavior in obese pediatric subjects. Subjects with more severe degrees of metabolic syndrome and obstructive sleep apnea syndrome showed larger reduction in nonlinear TPR baroreflex gain. Transfusion therapy in the sickle cell disease subjects led to an increase in nonlinear TPR baroreflex gain as well as the interaction between ABP and respiration.;In conclusion, through a combination of the structured and the minimal modeling approaches, we have developed an extended model of blood pressure variability that incorporates the respiratory modulation effect on R PV. Taking this respiratory modulation effect into account is important for achieving accurate TPR baroreflex estimation. Finally, the system gains derived from the estimated kernels may constitute potentially useful biomarkers of sympathetic nervous system function.
机译：据信，外周血管阻力（RPV）的调节很大程度上由交感神经介导。因此，对R PV控制的评估将使我们能够推断出有关交感神经活动的有价值的信息。 RPV的变化通常归因于总外周阻力（TPR）的压力反射控制。尽管已知呼吸会影响交感神经流出和深呼吸，就像叹息一样，会导致周围血管收缩，但是对TPR的呼吸调节作用却很少研究。在本研究中，我们利用RPV的无创替代措施来研究影响其变异性的两种机制：外周血管阻力的压力反射控制和呼吸-外周血管阻力耦合。第一种替代措施是从外周动脉眼压（PAT）获得的。 PAT测量了指尖处的音量变化，反映出血管收缩反应是其信号幅度的降低。另一种替代措施是从激光多普勒血流仪获得的，该多普勒血流仪监测微血管的灌注。这项研究的结果表明，RPV波动是通过呼吸直接调节的，而不是通过呼吸调节血压的间接作用来调节的。基于与短期血压调节相关的先前文献开发的模拟模型无法重现实验数据中观察到的叹气-血管收缩反应。采用最小建模方法来估计这种呼吸耦合效应，并将其纳入模拟模型。通过这两种建模方法，我们证明只有在将直接呼吸调节机制添加到仿真模型中后，叹气后才能再现类似的血管收缩反应;线性和非线性动力学以及相互作用的影响在输血治疗之前和之后，在暴露于体位压力的肥胖儿科患者和镰状细胞病患者中研究了通过ABP和呼吸变化对RPV的调节。在肥胖的小儿科目组中，我们发现由于体位性压力，TPR压力反射和呼吸耦合机制的线性增益均降低。这些增益的降低表明，尽管交感神经调升高，但是TPR的交感神经调节降低。体态应力被发现还导致肥胖儿科患者的非线性行为强度降低。代谢综合症和阻塞性睡眠呼吸暂停综合症程度较重的受试者显示出非线性TPR压力反射反射增益的更大降低。镰状细胞疾病受试者的输血治疗导致非线性TPR压力反射增益增加以及ABP与呼吸作用之间的相互作用。总之，通过结构化和最小化建模方法的结合，我们开发了扩展的模型血压变化，其中包括对R PV的呼吸调节作用。考虑到这种呼吸调节作用对于实现准确的TPR压力反射估计很重要。最后，从估计的核中获得的系统增益可能构成交感神经系统功能的潜在有用的生物标记。

著录项

  • 作者

    Chalacheva, Patjanaporn.;

  • 作者单位

    University of Southern California.;

  • 授予单位 University of Southern California.;
  • 学科 Engineering Biomedical.
  • 学位 Ph.D.
  • 年度 2014
  • 页码 214 p.
  • 总页数 214
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

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