...
首页> 外文期刊>Physiological Reports >Influence of CO2 on neurovascular coupling: interaction with dynamic cerebral autoregulation and cerebrovascular reactivity
【24h】

Influence of CO2 on neurovascular coupling: interaction with dynamic cerebral autoregulation and cerebrovascular reactivity

机译:CO2对神经血管耦合的影响:与动态脑自动调节和脑血管反应性的相互作用

获取原文
           

摘要

AbstractPaCO2 affects cerebral blood flow (CBF) and its regulatory mechanisms, but the interaction between neurovascular coupling (NVC), cerebral autoregulation (CA), and cerebrovascular reactivity to CO2 (CVR), in response to hypercapnia, is not known. Recordings of cerebral blood flow velocity (CBFv), blood pressure (BP), heart rate, and end-tidal CO2 (EtCO2) were performed in 18 subjects during normocapnia and 5% CO2 inhalation while performing a passive motor paradigm. Together with BP and EtCO2, a gate signal to represent the effect of stimulation was used as input to a multivariate autoregressive-moving average model to calculate their separate effects on CBFv. Hypercapnia led to a depression of dynamic CA at rest and during stimulation in both hemispheres (P  0.02) as well as impairment of the NVC response, particularly in the ipsilateral hemisphere (P  0.01). Neither hypercapnia nor the passive motor stimulation influenced CVR. Dynamic CA was not influenced by the motor paradigm during normocapnia. The CBFv step responses to each individual input (BP, EtCO2, stimulation) allowed identification of the influences of hypercapnia and neuromotor stimulation on CA, CVR, and NVC, which have not been previously described, and also confirmed the depressing effects of hypercapnia on CA and NVC. The stability of CVR during these maneuvers and the lack of influence of stimulation on dynamic CA are novel findings which deserve further investigation. Dynamic multivariate modeling can identify the complex interplay between different CBF regulatory mechanisms and should be recommended for studies involving similar interactions, such as the effects of exercise or posture on cerebral hemodynamics.
机译:摘要PaCO 2 影响脑血流量(CBF)及其调节机制,但神经血管偶联(NVC),脑自动调节(CA)和脑血管对CO 2 的反应性之间存在相互作用(CVR)对高碳酸血症的反应尚不清楚。在正常碳酸血症期间,对18位受试者进行了脑血流速度(CBFv),血压(BP),心率和潮气末CO 2 (EtCO 2 )的记录和5%的CO 2 吸入,同时执行被动运动模式。与BP和EtCO 2 一起,代表刺激效果的门信号被用作多元自回归移动平均模型的输入,以计算它们对CBFv的单独影响。高碳酸血症导致静息和刺激期间两个半球的动态CA降低(P <0.02)以及NVC反应的损害,特别是在同侧半球(P <0.01)。高碳酸血症和被动运动刺激均未影响CVR。动态CA在正常碳酸血症期间不受运动范式的影响。对每个单独输入(BP,EtCO 2 ,刺激)的CBFv阶跃响应可以识别出高碳酸血症和神经运动刺激对CA,CVR和NVC的影响,这在以前没有描述过,并且证实了高碳酸血症对CA和NVC的抑制作用。在这些演习中CVR的稳定性以及刺激对动态CA的影响缺乏是新发现,值得进一步研究。动态多变量建模可以识别不同CBF调节机制之间的复杂相互作用,因此建议将其推荐用于涉及相似相互作用的研究,例如运动或姿势对脑血流动力学的影响。

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