McCulloch Timothy J, Boesel Tillman W, Lam Arthur M
*Department of Anaesthetics, Royal Prince Alfred Hospital and †University of Sydney, Sydney, Australia; and ‡Department of Anesthesiology, University of Washington School of Medicine, Seattle, Washington.
Anesth Analg. 2005 May;100(5):1463-1467. doi: 10.1213/01.ANE.0000148623.06596.7E.
Isoflurane impairs autoregulation of cerebral blood flow in a dose-related manner. Previous investigations in several other conditions have demonstrated that impaired autoregulation can be restored by hyperventilation. We hypothesized that hypocapnia may restore cerebral autoregulation impaired by isoflurane anesthesia. We administered isoflurane in 100% oxygen to 12 healthy patients aged 21-59 yr scheduled for elective nonneurological surgery. Isoflurane end-tidal concentration was individualized at 0.1% to 0.2% less than that required to induce short periods of isoelectric electroencephalogram. This resulted in an end-tidal isoflurane concentration of 1.6% +/- 0.2% (mean +/- sd) corresponding to an age-adjusted minimum alveolar anesthetic concentration multiple of 1.4. Mean arterial blood pressure was reduced to <80 mm Hg, by infusion of remifentanil if required. Cerebral autoregulation was assessed by infusing phenylephrine to increase mean arterial blood pressure to 100 mm Hg while monitoring middle cerebral artery blood flow velocity with transcranial Doppler ultrasonography. The change in flow velocity was used to calculate the autoregulation index (ARI). The ARI ranges between 0 and 1 and an ARI < or =0.4 indicates significantly impaired autoregulation. Autoregulation was tested twice in randomized order: once during normocapnia (Paco(2) 38-43 mm Hg) and once during hypocapnia (Paco(2) 27-34 mm Hg). The median (interquartile range) ARI was 0.29 (0.23-0.64) during normocapnia and 0.77 (0.70-0.78) during hypocapnia (P < 0.005). Of the 12 subjects, autoregulation was significantly impaired in 8 subjects during normocapnia and none during hypocapnia (P = 0.001). Hypocapnia restored cerebral autoregulation in normal subjects during isoflurane-induced impairment of autoregulation.
异氟烷以剂量相关的方式损害脑血流的自动调节。先前在其他几种情况下的研究表明，过度通气可恢复受损的自动调节。我们假设低碳酸血症可能恢复异氟烷麻醉所致的脑自动调节受损。我们将异氟烷与100%氧气混合给予12例年龄在21 - 59岁、计划行择期非神经外科手术的健康患者。异氟烷呼气末浓度个体化设定为比诱导短时间脑电图等电位所需浓度低0.1%至0.2%。这导致呼气末异氟烷浓度为1.6%±0.2%（均值±标准差），相当于年龄校正的最低肺泡麻醉浓度倍数为1.4。必要时通过输注瑞芬太尼将平均动脉血压降至<80 mmHg。通过输注去氧肾上腺素将平均动脉血压升至100 mmHg，同时用经颅多普勒超声监测大脑中动脉血流速度来评估脑自动调节。流速变化用于计算自动调节指数（ARI）。ARI范围在0至1之间，ARI≤0.4表明自动调节明显受损。自动调节按随机顺序测试两次：一次在正常碳酸血症（动脉血二氧化碳分压38 - 43 mmHg）期间，一次在低碳酸血症（动脉血二氧化碳分压27 - 34 mmHg）期间。正常碳酸血症期间ARI的中位数（四分位间距）为0.29（0.23 - 0.64），低碳酸血症期间为0.77（0.70 - 0.78）（P < 0.005）。12名受试者中，8名受试者在正常碳酸血症期间自动调节明显受损，低碳酸血症期间无一人受损（P = 0.001）。低碳酸血症可恢复正常受试者在异氟烷诱导的自动调节受损期间的脑自动调节。
