Cerebral blood flow response to acute hypoxic hypoxia.
Cerebral blood flow response to acute hypoxic hypoxia.
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DOI：
10.1002/nbm.3026
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发表时间：
2013-12
影响因子：
2.9
通讯作者：
Wise, Richard G.
中科院分区：
文献类型：
--
作者：
Harris, Ashley D.;Murphy, Kevin;Diaz, Claris M.;Saxena, Neeraj;Hall, Judith E.;Liu, Thomas T.;Wise, Richard G.
关键词：
缺氧性缺氧（吸气性缺氧）刺激脑血流量（CBF）增加，维持向大脑输送氧气。然而，这种反应，特别是在组织水平，没有得到很好的表征。本研究量化了健康受试者对急性低氧缺氧的CBF反应。一个20分钟的缺氧（平均PETo 2 = 52毫米汞柱）的挑战，诱导和控制的动态潮气末迫使，而CBF测量使用脉冲动脉自旋标记灌注MRI。使用全脑和区域灰质的指数模型表征CBF响应的速率常数、时间延迟和幅度。灰质CBF从76.1 mL/100 g/min（拟合的95%置信区间（CI）：75.5 mL/100 g/min，76.7 mL/100 g/min）至87.8 mL/100 g/min（95%CI：86.7 mL/100 g/min，89.6 mL/100 g/min），对缺氧反应的时间延迟和速率常数为185 s（95%CI：132 s，230 s）和0.0035 s-1（95%CI：0.0019 s-1，0.0046 s-1）。从缺氧中恢复更快，延迟20 s（95% CI：-38 s，38 s），速率常数为0.0069 s-1（95% CI：0.0020 s-1，0.0103 s-1）。与CBF测量同时获得的血氧指数R2* 在缺氧时从30.33 s-1（CI：30.31 s-1，30.34 s-1）增加到31.48 s-1（CI：31.47 s-1，31.49 s-1）。R2* 变化的延迟和速率常数为24 s（95% CI：21 s，26 s）和0.0392 s-1（95%CI：0.0333 s-1，0.045 s-1），12 s（95% CI：10 s，13 s）和0.0921 s-1（95% CI：0.0744 s-1，0.1098 s-1/），证实了潮气末强制系统的血氧快速变化。CBF和R2* 对缺氧的反应性在受试者之间不同，但只有R2* 对缺氧的反应性在脑区之间有显著差异。© 2013作者。NMR in Biomedicine，John Wiley & Sons，Ltd.
Hypoxic hypoxia (inspiratory hypoxia) stimulates an increase in cerebral blood flow (CBF) maintaining oxygen delivery to the brain. However, this response, particularly at the tissue level, is not well characterised. This study quantifies the CBF response to acute hypoxic hypoxia in healthy subjects. A 20-min hypoxic (mean PETo2 = 52 mmHg) challenge was induced and controlled by dynamic end-tidal forcing whilst CBF was measured using pulsed arterial spin labelling perfusion MRI. The rate constant, temporal delay and magnitude of the CBF response were characterised using an exponential model for whole-brain and regional grey matter. Grey matter CBF increased from 76.1 mL/100 g/min (95% confidence interval (CI) of fitting: 75.5 mL/100 g/min, 76.7 mL/100 g/min) to 87.8 mL/100 g/min (95% CI: 86.7 mL/100 g/min, 89.6 mL/100 g/min) during hypoxia, and the temporal delay and rate constant for the response to hypoxia were 185 s (95% CI: 132 s, 230 s) and 0.0035 s–1 (95% CI: 0.0019 s–1, 0.0046 s–1), respectively. Recovery from hypoxia was faster with a delay of 20 s (95% CI: –38 s, 38 s) and a rate constant of 0.0069 s–1 (95% CI: 0.0020 s–1, 0.0103 s–1). R2*, an index of blood oxygenation obtained simultaneously with the CBF measurement, increased from 30.33 s–1 (CI: 30.31 s–1, 30.34 s–1) to 31.48 s–1 (CI: 31.47 s–1, 31.49 s–1) with hypoxia. The delay and rate constant for changes in R2* were 24 s (95% CI: 21 s, 26 s) and 0.0392 s–1 (95% CI: 0.0333 s–1, 0.045 s–1 ), respectively, for the hypoxic response, and 12 s (95% CI: 10 s, 13 s) and 0.0921 s–1 (95% CI: 0.0744 s–1, 0.1098 s–1/) during the return to normoxia, confirming rapid changes in blood oxygenation with the end-tidal forcing system. CBF and R2* reactivity to hypoxia differed between subjects, but only R2* reactivity to hypoxia differed significantly between brain regions. © 2013 The Authors. NMR in Biomedicine published by John Wiley & Sons, Ltd.
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DOI：
10.1038/jcbfm.2011.81
发表时间：
2011-10
期刊：
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism
影响因子：
--
作者：
通讯作者：
--
影响因子：
2.9
作者：
Noeth, Ulrike;Kotajima, Futoshi;Corfield, Douglas R.
通讯作者：
Corfield, Douglas R.
影响因子：
3.3
作者：
MacIntosh, Bradley J.;Filippini, Nicola;Jezzard, Peter
通讯作者：
Jezzard, Peter
影响因子：
5.7
作者：
Jenkinson, M;Bannister, P;Smith, S
通讯作者：
Smith, S
影响因子：
3.3
作者：
Poulin, MJ;Liang, PJ;Robbins, PA
通讯作者：
Robbins, PA