Wang Mei, Joshi Shailendra, Emerson Ronald G
Department of Anesthesiology, Columbia University, College of Physicians and Surgeons, New York, New York, USA.
Anesthesiology. 2003 Oct;99(4):904-10. doi: 10.1097/00000542-200310000-00024.
The high lipid solubility that permits rapid transfer across the blood-brain barrier makes propofol attractive for intracarotid injection. The authors hypothesized that intracarotid injection produces electrocerebral silence at a fraction of the intravenous dose and with less adverse systemic and cerebrovascular side effects.
The authors compared the systemic and cerebrovascular effects of intracarotid and intravenous propofol during transient (10 s) and sustained (1 h) electrocerebral silence in anesthetized New Zealand White rabbits. Hemispheric electrocerebral activity, mean arterial blood pressure, ipsilateral and contralateral cerebral blood flow, tympanic temperature, and end-tidal carbon dioxide were continuously monitored in these animals. Changes in outcome variables were analyzed at four time points: at baseline, during electrical silence, during burst suppression, and after recovery of electrocerebral activity. Propofol (1%) was injected as intracarotid (0.1 ml) or intravenous (0.5 ml) boluses.
Intracarotid propofol produced electrocerebral silence at one fifth (sustained silence) to one tenth (transient silence) of the intravenous dose. Compared with baseline values, the mean arterial pressure and ipsilateral cerebral blood flow remained unchanged or decreased transiently during electrocerebral silence with intracarotid propofol. In contrast, intravenous propofol resulted in systemic hypotension and a decrease in ipsilateral cerebral blood flow.
Intracarotid propofol resulted in electrocerebral silence at a fraction of the intravenous dose that was not associated with systemic hypotension or a sustained decrease in the cerebral blood flow. Intracarotid propofol could be potentially useful for providing electrocerebral silence when cerebral perfusion is at risk.
丙泊酚具有高脂质溶解性,可使其快速透过血脑屏障,这使得其用于颈内动脉注射颇具吸引力。作者推测,颈内动脉注射丙泊酚能以静脉注射剂量的一小部分产生脑电静息,且全身和脑血管的不良反应较少。
作者比较了在麻醉的新西兰白兔中,颈内动脉注射和静脉注射丙泊酚在短暂(10秒)和持续(1小时)脑电静息期间对全身和脑血管的影响。连续监测这些动物的半球脑电活动、平均动脉血压、同侧和对侧脑血流量、鼓膜温度和呼气末二氧化碳。在四个时间点分析结果变量的变化:基线、脑电静息期间、爆发抑制期间和脑电活动恢复后。以颈内动脉(0.1毫升)或静脉(0.5毫升)推注的方式注射1%的丙泊酚。
颈内动脉注射丙泊酚产生脑电静息所需剂量为静脉注射剂量的五分之一(持续静息)至十分之一(短暂静息)。与基线值相比,颈内动脉注射丙泊酚在脑电静息期间平均动脉压和同侧脑血流量保持不变或短暂下降。相比之下,静脉注射丙泊酚导致全身低血压和同侧脑血流量减少。
颈内动脉注射丙泊酚以静脉注射剂量的一小部分即可产生脑电静息,且与全身低血压或脑血流量持续减少无关。当脑灌注存在风险时,颈内动脉注射丙泊酚可能有助于实现脑电静息。