Liu Meizi, Jayaraman Keshav, Nelson James W, Mehla Jogender, Diwan Deepti, Vellimana Ananth K, Zipfel Gregory J, Athiraman Umeshkumar
Molecular Cell Biology, Washington University, St. Louis, MO 63110, USA.
Department of Neurological Surgery, Washington University, St. Louis, MO 63110, USA.
Diseases. 2023 Sep 27;11(4):130. doi: 10.3390/diseases11040130.
Delayed cerebral ischemia (DCI) is an important contributor to poor outcomes in aneurysmal subarachnoid hemorrhage (SAH) patients. We previously showed that volatile anesthetics such as isoflurane, sevoflurane and desflurane provided robust protection against SAH-induced DCI, but the impact of a more commonly used intravenous anesthetic agent, propofol, is not known. The goal of our current study is to examine the neurovascular protective effects of propofol on SAH-induced DCI. Twelve-week-old male wild-type mice were utilized for the study. Mice underwent endovascular perforation SAH or sham surgery followed one hour later by propofol infusion through the internal jugular vein (2 mg/kg/min continuous intravenous infusion). Large artery vasospasm was assessed three days after SAH. Neurological outcome assessment was performed at baseline and then daily until animal sacrifice. Statistical analysis was performed via one-way ANOVA and two-way repeated measures ANOVA followed by the Newman-Keuls multiple comparison test with significance set at < 0.05. Intravenous propofol did not provide any protection against large artery vasospasm or sensory-motor neurological deficits induced by SAH. Our data show that propofol did not afford significant protection against SAH-induced DCI. These results are consistent with recent clinical studies that suggest that the neurovascular protection afforded by anesthetic conditioning is critically dependent on the class of anesthetic agent.
迟发性脑缺血（DCI）是导致动脉瘤性蛛网膜下腔出血（SAH）患者预后不良的重要因素。我们之前的研究表明，异氟烷、七氟烷和地氟烷等挥发性麻醉剂对SAH诱导的DCI具有强大的保护作用，但一种更常用的静脉麻醉剂丙泊酚的影响尚不清楚。我们当前研究的目的是研究丙泊酚对SAH诱导的DCI的神经血管保护作用。本研究使用12周龄雄性野生型小鼠。小鼠接受血管内穿刺SAH或假手术，1小时后通过颈内静脉输注丙泊酚（2mg/kg/min持续静脉输注）。SAH后3天评估大动脉痉挛情况。在基线时进行神经功能结局评估，然后每天评估直至处死动物。通过单因素方差分析和双因素重复测量方差分析进行统计分析，随后进行Newman-Keuls多重比较检验，显著性设定为<0.05。静脉注射丙泊酚对SAH诱导的大动脉痉挛或感觉运动神经功能缺损没有提供任何保护作用。我们的数据表明，丙泊酚对SAH诱导的DCI没有显著的保护作用。这些结果与最近的临床研究一致，这些研究表明麻醉预处理提供的神经血管保护作用严重依赖于麻醉剂的种类。
