Kochs E, Hoffman W E, Werner C, Thomas C, Albrecht R F, Schulte am Esch J
Department of Anesthesiology, University Hospital Eppendorf, Hamburg, Germany.
Anesthesiology. 1992 Feb;76(2):245-52. doi: 10.1097/00000542-199202000-00014.
This study compares the effects of propofol and fentanyl/N2O on spontaneous brain electrical activity, neurologic outcome, and neuronal damage due to incomplete cerebral ischemia in rats. Thirty Sprague-Dawley rats were assigned to one of three groups: group 1 (n = 10) received 70% N2O in O2 plus fentanyl (bolus 10 micrograms.kg-1, infusion 25 micrograms.kg-1.h-1); group 2 (n = 10) received 70% N2 in O2 and propofol (infusion 0.8-1.2 mg.kg-1.min-1) adjusted to maintain EEG burst suppression during ischemia; group 3 (n = 10) was anesthetized with propofol and received 6 ml.kg-1 10% glucose intraperitoneally 15 min before the start of ischemia. Incomplete cerebral ischemia was produced by right common carotid artery occlusion combined with hemorrhagic hypotension (35 mmHg) for 30 min. Arterial blood gases, pH, and rectal temperature were kept constant in all groups. Plasma glucose was lower during ischemia in propofol-anesthetized rats compared to that in fentanyl/N2O- (P = 0.009) and glucose-loaded propofol-treated rats (P = 0.008). Neurologic outcome and brain tissue injury were significantly better in propofol-anesthetized compared to fentanyl/N2O-anesthetized rats (P less than 0.05). Elevated plasma glucose in propofol-treated rats resulted in similar neurologic outcome and histopathologic injury as seen in propofol-anesthetized rats given no glucose. Recovery of EEG theta-alpha activity after ischemia was inversely correlated to neurologic deficit (fentanyl/N2O: r = -0.71; propofol: r = -0.83; P less than 0.01). These results show that propofol improves neurologic outcome and decreases neuronal damage from incomplete cerebral ischemia when compared to fentanyl/N2O. This effect is not dependent on plasma glucose.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究比较了丙泊酚与芬太尼/氧化亚氮对大鼠自发性脑电活动、神经学转归以及不完全性脑缺血所致神经元损伤的影响。30只Sprague-Dawley大鼠被分为三组：第1组（n = 10）接受氧气中70%氧化亚氮加芬太尼（静脉推注10微克/千克，输注25微克/千克·小时）；第2组（n = 10）接受氧气中70%氮气和丙泊酚（输注0.8 - 1.2毫克/千克·分钟），调整剂量以在缺血期间维持脑电图爆发抑制；第3组（n = 10）用丙泊酚麻醉，并在缺血开始前15分钟腹腔注射6毫升/千克10%葡萄糖。通过右颈总动脉闭塞联合出血性低血压（35毫米汞柱）30分钟造成不完全性脑缺血。所有组的动脉血气、pH值和直肠温度均保持恒定。与芬太尼/氧化亚氮麻醉的大鼠（P = 0.009）和葡萄糖负荷丙泊酚处理的大鼠（P = 0.008）相比，丙泊酚麻醉的大鼠在缺血期间血浆葡萄糖水平较低。与芬太尼/氧化亚氮麻醉的大鼠相比，丙泊酚麻醉的大鼠神经学转归和脑组织损伤明显更好（P < 0.05）。丙泊酚处理的大鼠血浆葡萄糖升高导致的神经学转归和组织病理学损伤与未给予葡萄糖的丙泊酚麻醉大鼠相似。缺血后脑电图θ-α活动的恢复与神经功能缺损呈负相关（芬太尼/氧化亚氮：r = -0.71；丙泊酚：r = -0.83；P < 0.01）。这些结果表明，与芬太尼/氧化亚氮相比，丙泊酚可改善神经学转归并减少不完全性脑缺血所致的神经元损伤。这种作用不依赖于血浆葡萄糖。（摘要截短至250字）
