Dynamic cerebral autoregulation is intact in chronic kidney disease.
Dynamic cerebral autoregulation is intact in chronic kidney disease.
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DOI：
10.14814/phy2.15495
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发表时间：
2022-11
影响因子：
2.5
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中科院分区：
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慢性肾病（CKD）患者发生脑血管疾病的风险升高。可能导致这种风险升高的一个因素是动态脑自动调节功能受损，这是脑血管在动脉压波动期间调节脑血流量的机制。我们假设CKD患者的动态脑自动调节功能受损。为了验证这一假设，我们比较了III-IV期CKD患者和无CKD的匹配对照（CON）之间的动态脑自动调节。15名CKD患者和20名CON参与者在0.05 Hz和0.10 Hz下进行了2次5分钟的重复坐立运动，同时连续测量平均动脉压（MAP，通过手指光电体积描记法）和大脑中动脉血流速度（MCAv，通过经颅多普勒超声）。通过对MAP-MCAv关系进行传递函数分析（TFA）来表征大脑自动调节，以推导出相干性、相位、增益和归一化增益（nGain）。在重复的坐立动作中，我们没有观察到任何TFA指标的组间差异。在0.05 Hz操作期间，相干：CKD = 0.83 ± 0.13，CON = 0.85 ± 0.12，相位（弧度）：CKD = 1.39 ± 0.41，CON = 1.25 ± 0.30，增益（cm/s/mmHg）：CKD = 0.69 ± 0.20，CON = 0.71 ± 0.22，n增益（%/mmHg）：CKD = 1.26 ± 0.35，CON = 1.20 ± 0.28，p ≥ 0.24。在0.10 Hz操作期间（N = 6 CKD和N = 12 CON），相干性：CKD = 0.61 ± 0.10，CON = 0.67 ± 0.11，相位（弧度）：CKD = 1.43 ± 0.26，CON = 1.30 ± 0.23，增益（cm/s/mmHg）：CKD = 0.75 ± 0.15，CON = 0.84 ± 0.26，n增益（%/mmHg）：CKD = 1.50 ± 0.28，CON = 1.29 ± 0.24，p ≥ 0.12。与我们的假设相反，动态脑自动调节在CKD III-IV期中保持完整。这些结果表明，其他机制可能有助于增加脑血管疾病的负担，经历了这一人群。未来的工作应确定其他脑血管调节机制是否受损，以及是否与CKD患者的脑血管疾病风险相关。慢性肾病（CKD）患者发生脑血管疾病的风险升高，这可能部分由动态脑自动调节功能受损介导。我们比较了III-IV期CKD患者与无CKD的匹配对照（CON）之间的动态脑自动调节，并假设CKD患者的动态脑自动调节受损。与我们的假设相反，动态脑自动调节在CKD中保持完整，这表明其他机制可能导致该人群经历的脑血管疾病负担增加。
Chronic Kidney Disease (CKD) patients experience an elevated risk for cerebrovascular disease. One factor that may contribute to this heightened risk is an impairment in dynamic cerebral autoregulation, the mechanism by which cerebral vessels modulate cerebral blood flow during fluctuations in arterial pressure. We hypothesized that dynamic cerebral autoregulation would be impaired in CKD. To test this hypothesis, we compared dynamic cerebral autoregulation between CKD patients stages III‐IV and matched controls (CON) without CKD. Fifteen patients with CKD and 20 CON participants performed 2, 5‐minute bouts of repeated sit‐to‐stand maneuvers at 0.05 Hz and 0.10 Hz while mean arterial pressure (MAP, via finger photoplethysmography) and middle cerebral artery blood velocity (MCAv, via transcranial Doppler ultrasound) were measured continuously. Cerebral autoregulation was characterized by performing a transfer function analysis (TFA) on the MAP‐MCAv relationship to derive coherence, phase, gain, and normalized gain (nGain). We observed no group differences in any of the TFA metrics during the repeated sit‐to‐stand maneuvers. During the 0.05 Hz maneuver, Coherence: CKD = 0.83 ± 0.13, CON = 0.85 ± 0.12, Phase (radians): CKD = 1.39 ± 0.41, CON = 1.25 ± 0.30, Gain (cm/s/mmHg): CKD = 0.69 ± 0.20, CON = 0.71 ± 0.22, nGain (%/mmHg): CKD = 1.26 ± 0.35, CON = 1.20 ± 0.28, p ≥ 0.24. During the 0.10 Hz maneuver (N = 6 CKD and N = 12 CON), Coherence: CKD = 0.61 ± 0.10, CON = 0.67 ± 0.11, Phase (radians): CKD = 1.43 ± 0.26, CON = 1.30 ± 0.23, Gain (cm/s/mmHg): CKD = 0.75 ± 0.15, CON = 0.84 ± 0.26, nGain (%/mmHg): CKD = 1.50 ± 0.28, CON = 1.29 ± 0.24, p ≥ 0.12. Contrary to our hypothesis, dynamic cerebral autoregulation remains intact in CKD stages III‐IV. These findings suggest that other mechanisms likely contribute to the increased cerebrovascular disease burden experienced by this population. Future work should determine if other cerebrovascular regulatory mechanisms are impaired and related to cerebrovascular disease risk in CKD. Chronic Kidney Disease (CKD) patients experience an elevated risk for cerebrovascular disease, which may be mediated in part by an impairment in dynamic cerebral autoregulation. We compared dynamic cerebral autoregulation between CKD patients stages III‐IV vs matched controls (CON) without CKD and hypothesized that dynamic cerebral autoregulation would be impaired in CKD. Contrary to our hypothesis, dynamic cerebral autoregulation remains intact in CKD, which suggests that other mechanisms likely contribute to the increased cerebrovascular disease burden experienced by this population.