School of Health and Exercise Sciences, Faculty of Health and Social Development, University of British Columbia, Okanagan Campus, Canada, 3333 University Way, Kelowna, BC Canada V1V 1V7.
J Physiol. 2012 Jul 15;590(14):3261-75. doi: 10.1113/jphysiol.2012.228551. Epub 2012 Apr 10.
Despite the importance of blood flow on brainstem control of respiratory and autonomic function, little is known about regional cerebral blood flow (CBF) during changes in arterial blood gases.We quantified: (1) anterior and posterior CBF and reactivity through a wide range of steady-state changes in the partial pressures of CO2 (PaCO2) and O2 (PaO2) in arterial blood, and (2) determined if the internal carotid artery (ICA) and vertebral artery (VA) change diameter through the same range.We used near-concurrent vascular ultrasound measures of flow through the ICA and VA, and blood velocity in their downstream arteries (the middle (MCA) and posterior (PCA) cerebral arteries). Part A (n =16) examined iso-oxic changes in PaCO2, consisting of three hypocapnic stages (PaCO2 =∼15, ∼20 and ∼30 mmHg) and four hypercapnic stages (PaCO2 =∼50, ∼55, ∼60 and ∼65 mmHg). In Part B (n =10), during isocapnia, PaO2 was decreased to ∼60, ∼44, and ∼35 mmHg and increased to ∼320 mmHg and ∼430 mmHg. Stages lasted ∼15 min. Intra-arterial pressure was measured continuously; arterial blood gases were sampled at the end of each stage. There were three principal findings. (1) Regional reactivity: the VA reactivity to hypocapnia was larger than the ICA, MCA and PCA; hypercapnic reactivity was similar.With profound hypoxia (35 mmHg) the relative increase in VA flow was 50% greater than the other vessels. (2) Neck vessel diameters: changes in diameter (∼25%) of the ICA was positively related to changes in PaCO2 (R2, 0.63±0.26; P<0.05); VA diameter was unaltered in response to changed PaCO2 but yielded a diameter increase of +9% with severe hypoxia. (3) Intra- vs. extra-cerebral measures: MCA and PCA blood velocities yielded smaller reactivities and estimates of flow than VA and ICA flow. The findings respectively indicate: (1) disparate blood flow regulation to the brainstem and cortex; (2) cerebrovascular resistance is not solely modulated at the level of the arteriolar pial vessels; and (3) transcranial Doppler ultrasound may underestimate measurements of CBF during extreme hypoxia and/or hypercapnia.
尽管血流对脑干控制呼吸和自主功能很重要，但人们对动脉血气变化期间的局部脑血流 (CBF) 知之甚少。我们定量测量了：(1) 在动脉血二氧化碳分压 (PaCO2) 和氧分压 (PaO2) 的稳态范围内，前脑和后脑的 CBF 和反应性；(2) 确定颈内动脉 (ICA) 和椎动脉 (VA) 是否通过相同范围改变直径。我们使用经颅超声测量 ICA 和 VA 的流量以及其下游动脉（大脑中动脉 (MCA) 和大脑后动脉 (PCA)）的血流速度。A 部分（n =16）检查了 PaCO2 的等氧变化，包括三个低碳酸血症阶段（PaCO2 =∼15、∼20 和 ∼30 mmHg）和四个高碳酸血症阶段（PaCO2 =∼50、∼55、∼60 和 ∼65 mmHg）。在 B 部分（n =10）中，在等碳酸血症期间，PaO2 降低至 ∼60、∼44 和 ∼35 mmHg，升高至 ∼320 mmHg 和 ∼430 mmHg。每个阶段持续约 15 分钟。连续测量动脉内压；在每个阶段结束时取样动脉血气。有三个主要发现。(1) 区域反应性：VA 对低碳酸血症的反应性大于 ICA、MCA 和 PCA；高碳酸血症反应性相似。在严重缺氧（35 mmHg）下，VA 流量的相对增加比其他血管高 50%。(2) 颈部血管直径：ICA 直径的变化（∼25%）与 PaCO2 的变化呈正相关（R2，0.63±0.26；P<0.05）；VA 直径对 PaCO2 的变化没有反应，但在严重缺氧时会增加 +9%。(3) 颅内与颅外测量：MCA 和 PCA 的血流速度产生的反应性和流量估计小于 VA 和 ICA 的血流速度。这些发现分别表明：(1) 脑干和皮质的血流调节不同；(2) 脑血管阻力不仅仅在血管内皮血管水平上调节；(3) 经颅多普勒超声可能低估了严重缺氧和/或高碳酸血症期间 CBF 的测量。
