Shibuya Kazuhiro, Ishiyama Tadahiko, Ichikawa Manabu, Sato Hiroaki, Okuyama Katsumi, Sessler Daniel I, Matsukawa Takashi
Department of Anesthesiology, Faculty of Medicine, University of Yamanashi, Yamanashi, Japan.
J Neurosurg Anesthesiol. 2009 Jan;21(1):40-6. doi: 10.1097/ANA.0b013e31818b22d5.
Propofol is widely used for neurosurgical anesthesia; however, its effects on the pial microvasculature are unknown. We therefore evaluated the direct effects of propofol on pial microvessels in rabbits. Pial microcirculation was visualized using a closed cranial window technique in 20 Japanese white rabbits. In the first experiment (n=14), after baseline hemodynamic measurements, the cranial window was superfused with 5 increasing concentrations of propofol (10, 10, 10, 10, 10 mol/L; n=8) or intralipid (at comparable concentrations; n=6) dissolved in artificial cerebrospinal fluid for 7 minutes each. A typical anesthetic concentration of 5 microg/mL corresponds to 10 mol/L. In the second experiment (n=6), phenylephrine 10 mol/L and nitroglycerin 10 mol/L were applied topically for 7 minutes under pentobarbital anesthesia. In the third experiment (n=3), electroencephalogram and bispectral index were measured under pentobarbital anesthesia. Diameters of selected pial arterioles and venules were visualized with a microscope-video capture unit combination and subsequently measured with a digital video analyzer. Topical application of propofol at 10, 10, 10, or 10 mol/L did not alter the diameters of the pial microvessels; however, at 10 mol/L propofol induced dilation in large and small arterioles, along with venular dilation. Intralipid alone did not have any significant effect on vessel diameters. Phenylephrine and nitroglycerin produced pial arteriolar and venular constriction and dilation, respectively. Phenylephrine constricted and nitroglycerin dilated pial arterioles and venules. Pentobarbital did not produce either burst suppression or an isoelectric electroencephalogram. The results confirm our hypothesis: clinically relevant concentrations of propofol, that is, approximately 10 mol/L, do not dilate pial arterioles or venules.
丙泊酚广泛用于神经外科麻醉;然而,其对软脑膜微血管的影响尚不清楚。因此,我们评估了丙泊酚对兔软脑膜微血管的直接作用。采用封闭颅窗技术在20只日本白兔中观察软脑膜微循环。在第一个实验(n = 14)中,在进行基线血流动力学测量后,用5种递增浓度(10、10、10、10、10 μmol/L;n = 8)的丙泊酚或溶解于人工脑脊液中的等浓度脂质乳剂(n = 6)对颅窗进行灌注,每次灌注7分钟。5 μg/mL的典型麻醉浓度相当于10 μmol/L。在第二个实验(n = 6)中,在戊巴比妥麻醉下局部应用10 μmol/L的去氧肾上腺素和10 μmol/L的硝酸甘油7分钟。在第三个实验(n = 3)中,在戊巴比妥麻醉下测量脑电图和脑电双频指数。用显微镜 - 视频采集单元组合观察选定的软脑膜小动脉和小静脉的直径,随后用数字视频分析仪进行测量。局部应用10、10、10或10 μmol/L的丙泊酚不会改变软脑膜微血管的直径;然而,在10 μmol/L时,丙泊酚可引起大小动脉扩张以及小静脉扩张。单独的脂质乳剂对血管直径没有任何显著影响。去氧肾上腺素和硝酸甘油分别引起软脑膜小动脉收缩和小静脉扩张。去氧肾上腺素使软脑膜小动脉收缩,硝酸甘油使软脑膜小动脉和小静脉扩张。戊巴比妥既未产生爆发抑制也未产生脑电图等电位。结果证实了我们的假设:临床相关浓度的丙泊酚,即约10 μmol/L,不会使软脑膜小动脉或小静脉扩张。