From the Departments of Radiology (V.C.K., F.T., W.B., H.H.S., E.H.)
Anesthesiology and Intensive Care Medicine (L.E.).
AJNR Am J Neuroradiol. 2018 Oct;39(10):1839-1847. doi: 10.3174/ajnr.A5790. Epub 2018 Sep 20.
Experienced freedivers can endure prolonged breath-holds despite severe hypoxemia and are therefore ideal subjects to study apnea-induced cerebrovascular reactivity. This multiparametric study investigated CBF, the spatial coefficient of variation as a correlate of arterial transit time and brain metabolism, dynamics during prolonged apnea.
Fifteen male freedivers (age range, 20-64 years; cumulative previous prolonged breath-holds >2 minutes and 30 seconds: 4-79,200) underwent repetitive 3T pseudocontinuous arterial spin-labeling and P-/H-MR spectroscopy before, during, and after a 5-minute breath-hold (split into early and late phases) and gave temporally matching venous blood gas samples. Correlation of temporal and regional cerebrovascular reactivity to blood gases and cumulative previous breath-holds of >2 minutes and 30 seconds in a lifetime was assessed.
The spatial coefficient of variation of CBF (by arterial spin-labeling) decreased during the early breath-hold phase (-30.0%, = .002), whereas CBF remained almost stable during this phase and increased in the late phase (+51.8%, = .001). CBF differed between the anterior and the posterior circulation during all phases (eg, during late breath-hold: MCA, 57.3 ± 14.2 versus posterior cerebral artery, 42.7 ± 10.8 mL/100 g/min; = .001). There was an association between breath-hold experience and lower CBF (1000 previous breath-holds reduced WM CBF by 0.6 mL/100 g/min; 95% CI, 0.15-1.1 mL/100 g/min; = .01). While breath-hold caused peripheral lactate rise (+18.5%) and hypoxemia (oxygen saturation, -24.0%), cerebral lactate and adenosine diphosphate remained within physiologic ranges despite early signs of oxidative stress [-6.4% phosphocreatine / (adenosine triphosphate + adenosine diphosphate); = .02].
This study revealed that the cerebral energy metabolism of trained freedivers withstands severe hypoxic hypercarbia in prolonged breath-hold due to a complex cerebrovascular hemodynamic response.
有经验的自由潜水员可以在严重低氧血症的情况下长时间憋气,因此是研究 apnea-induced 脑血管反应性的理想对象。这项多参数研究调查了 CBF、作为动脉传输时间和脑代谢相关指标的空间变异系数、长时间 apnea 期间的动力学变化。
15 名男性自由潜水员(年龄 20-64 岁;累积之前的长时间憋气 >2 分钟和 30 秒:4-79,200)在 5 分钟的憋气(分为早期和晚期两个阶段)前、中、后接受了重复的 3T 伪连续动脉自旋标记和 P-/H-MR 光谱检查,并同时采集了时间匹配的静脉血气样本。评估了在整个生命过程中,时空脑血管反应性与血气和 >2 分钟和 30 秒的累积前期憋气之间的相关性。
早期憋气阶段,CBF(通过动脉自旋标记)的空间变异系数下降(-30.0%, =.002),而 CBF 在这个阶段几乎保持稳定,并在晚期阶段增加(+51.8%, =.001)。在所有阶段,CBF 在前后循环之间都存在差异(例如,在晚期憋气时:MCA,57.3 ± 14.2 与大脑后动脉,42.7 ± 10.8 mL/100 g/min; =.001)。憋气经验与较低的 CBF 之间存在关联(1000 次前期憋气使 WM CBF 降低 0.6 mL/100 g/min;95%CI,0.15-1.1 mL/100 g/min; =.01)。尽管出现了早期氧化应激迹象[-6.4%磷酸肌酸/(三磷酸腺苷+二磷酸腺苷); =.02],但由于复杂的脑血管血流动力学反应,训练有素的自由潜水员的脑能量代谢在长时间憋气时能够耐受严重的低氧高碳酸血症,导致外周血乳酸升高(+18.5%)和低氧(氧饱和度,-24.0%)。
这项研究表明,由于复杂的脑血管血流动力学反应,受过训练的自由潜水员的脑能量代谢可以在长时间的憋气中耐受严重的低氧高碳酸血症。