van Helmond Noud, Johnson Blair D, Holbein Walter W, Petersen-Jones Humphrey G, Harvey Ronée E, Ranadive Sushant M, Barnes Jill N, Curry Timothy B, Convertino Victor A, Joyner Michael J
Department of Anesthesiology, Mayo Clinic, Rochester, Minnesota.
Center for Research and Education in Special Environments, Department of Exercise and Nutrition Sciences, University at Buffalo, Buffalo, New York.
Physiol Rep. 2018 Feb;6(4). doi: 10.14814/phy2.13594.
The ability to maintain adequate cerebral blood flow and oxygenation determines tolerance to central hypovolemia. We tested the hypothesis that acute hypoxemia during simulated blood loss in humans would cause impairments in cerebral blood flow control. Ten healthy subjects (32 ± 6 years, BMI 27 ± 2 kg·m ) were exposed to stepwise lower body negative pressure (LBNP, 5 min at 0, -15, -30, and -45 mmHg) during both normoxia and hypoxia (F O = 0.12-0.15 O titrated to an SaO of ~85%). Physiological responses during both protocols were expressed as absolute changes from baseline, one subject was excluded from analysis due to presyncope during the first stage of LBNP during hypoxia. LBNP induced greater reductions in mean arterial pressure during hypoxia versus normoxia (MAP, at -45 mmHg: -20 ± 3 vs. -5 ± 3 mmHg, P < 0.01). Despite differences in MAP, middle cerebral artery velocity responses (MCAv) were similar between protocols (P = 0.41) due to increased cerebrovascular conductance index (CVCi) during hypoxia (main effect, P = 0.04). Low frequency MAP (at -45 mmHg: 17 ± 5 vs. 0 ± 5 mmHg , P = 0.01) and MCAv (at -45 mmHg: 4 ± 2 vs. -1 ± 1 cm·s , P = 0.04) spectral power density, as well as low frequency MAP-mean MCAv transfer function gain (at -30 mmHg: 0.09 ± 0.06 vs. -0.07 ± 0.06 cm·s ·mmHg , P = 0.04) increased more during hypoxia versus normoxia. Contrary to our hypothesis, these findings support the notion that cerebral blood flow control is not impaired during exposure to acute hypoxia and progressive central hypovolemia despite lower MAP as a result of compensated increases in cerebral conductance and flow variability.
维持充足脑血流量和氧合的能力决定了对中枢性低血容量的耐受性。我们检验了这样一个假设：人类在模拟失血过程中出现的急性低氧血症会导致脑血流控制受损。10名健康受试者（年龄32±6岁，体重指数27±2kg·m²）在常氧和低氧（FIO₂=0.12 - 0.15，将氧饱和度滴定至约85%）状态下均接受逐步降低的下体负压（LBNP，在0、-15、-30和-45mmHg下各持续5分钟）。两种方案期间的生理反应均表示为相对于基线的绝对变化，一名受试者因在低氧状态下LBNP第一阶段出现前驱晕厥而被排除在分析之外。与常氧相比，低氧状态下LBNP导致平均动脉压下降幅度更大（平均动脉压，在-45mmHg时：-20±3 vs. -5±3mmHg，P<0.01）。尽管平均动脉压存在差异，但由于低氧期间脑血管传导指数（CVCi）增加（主要效应，P=0.04），两种方案期间大脑中动脉血流速度反应（MCAv）相似（P=0.41）。低频平均动脉压（在-45mmHg时：17±5 vs. 0±5mmHg，P=0.01）和MCAv（在-45mmHg时：4±2 vs. -1±1cm·s，P=0.04）的频谱功率密度，以及低频平均动脉压-平均MCAv传递函数增益（在-30mmHg时：0.09±0.06 vs. -0.07±0.06cm·s·mmHg，P=0.04）在低氧状态下比常氧状态下增加得更多。与我们的假设相反，这些发现支持这样一种观点：尽管由于脑电导和血流变异性的代偿性增加导致平均动脉压降低，但在暴露于急性低氧血症和进行性中枢性低血容量期间，脑血流控制并未受损。
