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Supplementary Material for: Dynamics of critical closing pressure explain cerebral autoregulation impairment in acute cerebrovascular disease

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NIAID Data Ecosystem2026-05-02 收录
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https://figshare.com/articles/dataset/Supplementary_Material_for_Dynamics_of_critical_closing_pressure_explain_cerebral_autoregulation_impairment_in_acute_cerebrovascular_disease/26172343
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Introduction: Cerebral autoregulation (CA) is impaired in acute ischemic stroke (AIS) and is associated with worse patient outcomes, but the underlying physiological cause is unclear. This study tests whether depressed CA in AIS can be linked to the dynamic responses of critical closing pressure (CrCP) and resistance area product (RAP). Methods: Continuous recordings of middle cerebral blood velocity (MCAv, transcranial Doppler), arterial blood pressure (BP), end-tidal CO2 and electrocardiography allowed dynamic analysis of the instantaneous MCAv-BP relationship to obtain estimates of CrCP and RAP. The dynamic response of CrCP and RAP to a sudden change in mean BP was obtained by transfer function analysis. Comparisons were made between younger controls (≤50 years), older controls (>50 years), and AIS patients. Results: Data from 24 younger controls (36.4 ± 10.9 years, 9 male), 38 older controls (64.7 ± 8.2 years, 20 male), and 20 AIS patients (63.4 ± 13.8 years, 9 male) were included. Dynamic CA was impaired in AIS, with lower autoregulation index (affected hemisphere: 4.0 ± 2.3, unaffected: 4.5 ± 1.8) compared to younger (right: 5.8 ± 1.4, left: 5.8 ± 1.4) and older (right: 4.9 ± 1.6, left: 5.1 ± 1.5) controls. AIS patients also demonstrated an early (0-3 second) peak in CrCP dynamic response, that was not influenced by age. Conclusion: These early transient differences in the CrCP dynamic response are a novel finding in stroke and occur too early to reflect underlying regulatory mechanisms. Instead, these may be caused by structural changes to cerebral vasculature.

引言:脑自动调节(Cerebral autoregulation,CA)在急性缺血性卒中(acute ischemic stroke,AIS)中受损,且与患者不良预后相关,但其潜在生理机制尚未明确。本研究旨在探讨急性缺血性卒中患者的脑自动调节受损是否与临界闭合压(critical closing pressure,CrCP)及阻力面积乘积(resistance area product,RAP)的动态反应相关。 方法:通过连续记录大脑中动脉血流速度(middle cerebral blood velocity,MCAv,经颅多普勒)、动脉血压(arterial blood pressure,BP)、呼气末二氧化碳及心电图,对瞬时MCAv-BP关系进行动态分析,以估算临界闭合压与阻力面积乘积。通过传递函数分析,获取平均动脉血压骤变时临界闭合压与阻力面积乘积的动态反应。对年轻对照组(≤50岁)、老年对照组(>50岁)及急性缺血性卒中患者进行分组比较。 结果:本研究共纳入24名年轻对照组受试者(年龄36.4±10.9岁,男性9名)、38名老年对照组受试者(年龄64.7±8.2岁,男性20名)以及20名急性缺血性卒中患者(年龄63.4±13.8岁,男性9名)。急性缺血性卒中患者的动态脑自动调节受损,其脑自动调节指数(autoregulation index)在受累半球为4.0±2.3、非受累半球为4.5±1.8,均低于年轻对照组(右侧半球:5.8±1.4,左侧半球:5.8±1.4)与老年对照组(右侧半球:4.9±1.6,左侧半球:5.1±1.5)。此外,急性缺血性卒中患者的临界闭合压动态反应呈现早期(0~3秒)峰值,且该峰值不受年龄影响。 结论:临界闭合压动态反应的早期瞬时差异是卒中领域的全新发现,其发生时机过早,无法反映潜在的调节机制。此类差异或由脑血管结构改变所引发。
创建时间:
2024-07-04
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