Centre for Heart, Lung and Vascular Health, School of Health and Exercise Sciences, University of British Columbia Okanagan, Kelowna, BC, Canada.
Department of Anesthesiology, Pharmacology and Therapeutics, Vancouver General Hospital, University of British Columbia, Vancouver, BC, Canada.
J Physiol. 2021 Mar;599(5):1439-1457. doi: 10.1113/JP280682. Epub 2021 Jan 18.
We investigated the influence of arterial ( ) with and without acutely elevated arterial pH and bicarbonate ([HCO ]) on cerebral blood flow (CBF) regulation in the internal carotid artery and vertebral artery. We assessed stepwise iso-oxic alterations in (i.e. cerebrovascular CO reactivity) prior to and following i.v. sodium bicarbonate infusion (NaHCO ) to acutely elevate arterial pH and [HCO ]. Total CBF was unchanged irrespective of a higher arterial pH at each matched stage of , indicating that CBF is acutely regulated by rather than arterial pH. The cerebrovascular responses to changes in arterial H /pH were altered in keeping with the altered relationship between and H /pH following NaHCO infusion (i.e. changes in buffering capacity). Total CBF was ∼7% higher following NaHCO infusion during isocapnic breathing providing initial evidence for a direct vasodilatory influence of HCO independent of levels.
Cerebral blood flow (CBF) regulation is dependent on the integrative relationship between arterial ( ), pH and cerebrovascular tone; however, pre-clinical studies indicate that intrinsic sensitivity to pH, independent of changes in or intravascular bicarbonate ([HCO ]), principally influences cerebrovascular tone. Eleven healthy males completed a standardized cerebrovascular CO reactivity (CVR) test utilizing radial artery catheterization and Duplex ultrasound (CBF); consisting of matched stepwise iso-oxic alterations in (hypocapnia: -5, -10 mmHg; hypercapnia: +5, +10 mmHg) prior to and following i.v. sodium bicarbonate (NaHCO ; 8.4%, 50 mEq 50 mL ) to elevate pH (7.408 ± 0.020 vs. 7.461 ± 0.030; P < 0.001) and [HCO ] (26.1 ± 1.4 vs. 29.3 ± 0.9 mEq L ; P < 0.001). Absolute CBF was not different at each stage of CO reactivity (P = 0.629) following NaHCO , irrespective of a higher pH (P < 0.001) at each matched stage of (P = 0.927). Neither hypocapnic (3.44 ± 0.92 vs. 3.44 ± 1.05% per mmHg ; P = 0.499), nor hypercapnic (7.45 ± 1.85 vs. 6.37 ± 2.23% per mmHg ; P = 0.151) reactivity to were altered pre- to post-NaHCO . When indexed against arterial [H ], the relative hypocapnic CVR was higher (P = 0.019) and hypercapnic CVR was lower (P = 0.025) following NaHCO , respectively. These changes in reactivity to [H ] were, however, explained by alterations in buffering between and arterial H /pH consequent to NaHCO . Lastly, CBF was higher (688 ± 105 vs. 732 ± 89 mL min , 7% ± 12%; P = 0.047) following NaHCO during isocapnic breathing providing support for a direct influence of HCO on cerebrovascular tone independent of . These data indicate that in the setting of acute metabolic alkalosis, CBF is regulated by rather than arterial pH.
我们研究了在动脉 pH 和碳酸氢盐 ([HCO3-]) 急性升高的情况下，动脉（）对颈内动脉和椎动脉脑血流 (CBF) 调节的影响。我们评估了在静脉注射碳酸氢钠 (NaHCO3) 急性升高动脉 pH 和 [HCO3-] 之前和之后，逐步等氧改变（即脑血管 CO 反应性）。在每个匹配的阶段，尽管动脉 pH 较高，但总 CBF 保持不变，表明 CBF 是由而不是动脉 pH 急性调节的。在 NaHCO3 输注后，动脉 H /pH 变化的脑血管反应发生改变，与 NaHCO3 输注后（即缓冲能力改变）与之间的改变关系一致。在等碳酸呼吸期间，NaHCO3 输注后总 CBF 增加了约 7%，为 HCO3 独立于水平直接扩张血管的影响提供了初步证据。
脑血流 (CBF) 调节依赖于动脉（）、pH 和脑血管张力之间的综合关系；然而，临床前研究表明，对 pH 的固有敏感性，独立于或血管内碳酸氢盐 ([HCO3-]) 的变化，主要影响脑血管张力。11 名健康男性利用桡动脉导管和双功能超声（CBF）完成了标准化脑血管 CO 反应性 (CVR) 测试；包括在静脉注射碳酸氢钠 (NaHCO3；8.4%，50 mEq 50 mL) 之前和之后，逐步等氧改变（低碳酸血症：-5，-10mmHg；高碳酸血症：+5，+10mmHg），以升高 pH（7.408 ± 0.020 与 7.461 ± 0.030；P < 0.001）和 [HCO3-]（26.1 ± 1.4 与 29.3 ± 0.9 mEq L；P < 0.001）。在 NaHCO3 后，在 CO 反应性的每个阶段，绝对 CBF 没有差异（P = 0.629），尽管在每个匹配的阶段，pH 更高（P < 0.001）（P = 0.927）。在 NaHCO3 之前和之后，低碳酸血症（3.44 ± 0.92 与 3.44 ± 1.05% per mmHg；P = 0.499）和高碳酸血症（7.45 ± 1.85 与 6.37 ± 2.23% per mmHg；P = 0.151）对的反应性均未改变。当与动脉 [H] 相比时，相对低碳酸血症 CVR 更高（P = 0.019），高碳酸血症 CVR 更低（P = 0.025），分别在 NaHCO3 后。然而，这些对 [H] 的反应性变化是由于 NaHCO3 导致与动脉 H /pH 之间的缓冲变化。最后，在等碳酸呼吸期间，CBF 更高（688 ± 105 与 732 ± 89 mL min，7% ± 12%；P = 0.047），为 HCO3 独立于独立于的脑血管张力的直接影响提供了支持。这些数据表明，在急性代谢性碱中毒的情况下，CBF 是由而不是动脉 pH 调节的。
