Perry Blake G, Lucas Samuel J E, Thomas Kate N, Cochrane Darryl J, Mündel Toby
School of Sport and Exercise, Massey University, Palmerston North, New Zealand.
School of Sport, Exercise and Rehabilitation Sciences, College of Life and Environmental Sciences, University of Birmingham, Birmingham, UK Department of Physiology, University of Otago, Dunedin, New Zealand School of Physical Education, Sport and Exercise Sciences, University of Otago, Dunedin, New Zealand.
Physiol Rep. 2014 Jun 27;2(6). doi: 10.14814/phy2.12059. Print 2014 Jun 1.
Hypercapnia impairs cerebrovascular control during rapid changes in blood pressure (BP); however, data concerning the effect of hypercapnia on steady state, nonpharmacological increases in BP is scarce. We recruited fifteen healthy volunteers (mean ± SD: age, 28 ± 6 years; body mass, 77 ± 12 kg) to assess the effect of hypercapnia on cerebrovascular control during steady-state elevations in mean arterial BP (MAP), induced via lower body positive pressure (LBPP). Following 20 min of supine rest, participants completed 5 min of eucapnic 20 and 40 mm Hg LBPP (order randomized) followed by 5 min of hypercapnia (5% CO2 in air) with and without LBPP (order randomized), and each stage was separated by ≥5 min to allow for recovery. Middle cerebral artery blood velocity (MCAv), BP, partial pressure of end-tidal carbon dioxide (PETCO2) and heart rate were recorded and presented as the change from the preceding baseline. No difference in MCAv was apparent between eupcapnic baseline and LBPPs (grouped mean 65 ± 11 cm·s(-1), all P > 0.05), despite the increased MAP with LBPP (Δ6 ± 5 and Δ8 ± 3 mm Hg for 20 and 40 mm Hg, respectively, both P < 0.001 vs. baseline). Conversely, MCAv during the hypercapnic +40 mm Hg stage (Δ31 ± 13 cm·s(-1)) was greater than hypercapnia alone (Δ25 ± 11 cm·s(-1), P = 0.026), due to an increased MAP (Δ14 ± 7 mm Hg, P < 0.001 vs. hypercapnia alone and P = 0.026 vs. hypercapnia +20 mm Hg). As cardiac output and PETCO2 were similar across all hypercapnic stages (all P > 0.05), our findings indicate that hypercapnia impairs static autoregulation, such that higher blood pressures are translated into the cerebral circulation.
高碳酸血症在血压（BP）快速变化期间会损害脑血管调节；然而，关于高碳酸血症对稳态、非药物性血压升高影响的数据却很少。我们招募了15名健康志愿者（平均±标准差：年龄，28±6岁；体重，77±12千克），以评估高碳酸血症对通过下体正压（LBPP）诱导的平均动脉压（MAP）稳态升高期间脑血管调节的影响。在仰卧休息20分钟后，参与者完成了5分钟的正常碳酸水平下20和40毫米汞柱的LBPP（顺序随机），随后是5分钟有或无LBPP（顺序随机）的高碳酸血症（空气中5%二氧化碳），每个阶段间隔≥5分钟以允许恢复。记录大脑中动脉血流速度（MCAv）、血压、呼气末二氧化碳分压（PETCO2）和心率，并表示为相对于先前基线的变化。正常碳酸水平基线和LBPP之间MCAv无明显差异（分组平均值65±11厘米·秒⁻¹，所有P>0.05），尽管LBPP时MAP升高（20和40毫米汞柱时分别为Δ6±5和Δ8±3毫米汞柱，两者与基线相比P<0.001）。相反，高碳酸血症+40毫米汞柱阶段的MCAv（Δ31±13厘米·秒⁻¹）大于单独高碳酸血症时（Δ25±11厘米·秒⁻¹，P = 0.026），这是由于MAP升高（Δ14±7毫米汞柱，与单独高碳酸血症相比P<0.001，与高碳酸血症+20毫米汞柱相比P = 0.026）。由于所有高碳酸血症阶段的心输出量和PETCO2相似（所有P>0.05），我们的研究结果表明高碳酸血症会损害静态自动调节，从而使较高的血压传递到脑循环中。
