The effects of large-dose propofol on cerebrovascular pressure autoregulation in head-injured patients
The effects of large-dose propofol on cerebrovascular pressure autoregulation in head-injured patients
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DOI：
10.1213/01.ane.0000070234.17226.b0
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发表时间：
2003-08-01
影响因子：
5.7
通讯作者：
Menon, DK
中科院分区：
文献类型：
--
作者：
Steiner, LA;Johnston, AJ;Menon, DK
在健康个体中，输注异丙酚时，脑血管压力自动调节功能得以保留甚至改善。我们研究了 10 名头部受伤患者中丙泊酚血浆浓度增加对压力自动调节的影响。使用目标控制输注，在中等（2.3+/-0.4μg/mL）和大（4.3+/-0.04μg/mL）丙泊酚血浆目标浓度下确定自动调节的静态速率。使用去甲肾上腺素控制脑灌注压，在每个异丙酚浓度下脑灌注压为 70 和 85 mm Hg 时进行大脑中动脉经颅多普勒测量。大丙泊酚浓度下的大脑中动脉血流速度显着低于中等浓度下的血流速度，而动脉-颈静脉的氧含量差异没有同时增加，这一发现与维持的血流-代谢耦合相一致。尽管如此，静态自动调节率从 54% +/- 36% 显着下降至 28% +/- 35% (P = 0.029)。我们的数据表明，头部受伤后，异丙酚对脑血管的影响与在健康个体中观察到的不同。我们建议，对于头部受伤的患者应谨慎使用大剂量的异丙酚，因为这可能会增加受伤大脑对继发性损伤的脆弱性。
In healthy individuals, cerebrovascular pressure autoregulation is preserved or even improved when propofol is infused. We examined the effect of an increase in propofol plasma concentration on pressure autoregulation in 10 head-injured patients. Using target-controlled infusions, the static rate of autoregulation was determined at a moderate (2.3 +/- 0.4 mug/mL) and a large (4.3 +/- 0.04 mug/mL) plasma target concentration of propofol. Using norepinephrine to control cerebral perfusion pressure, transcranial Doppler measurements from the middle cerebral artery were made at a cerebral perfusion pressure of 70 and 85 mm Hg at each propofol concentration. Middle cerebral artery flow velocities at the large propofol concentration were significantly lower than at the moderate concentration, without any concurrent increase in arterio-jugular difference in oxygen content, a finding compatible with maintained flow-metabolism coupling. Despite this, static rate of autoregulation decreased significantly from 54% +/- 36% to 28% +/- 35% (P = 0.029). Our data suggest that after head injury, the cerebrovascular effects of propofol are different from those observed in healthy individuals. We propose that large doses of propofol should be used cautiously in head-injured patients, because there is the potential to increase the injured brain's vulnerability to secondary insults.