Propofol Affords No Protection against Delayed Cerebral Ischemia in a Mouse Model of Subarachnoid Hemorrhage.

Propofol Affords No Protection against Delayed Cerebral Ischemia in a Mouse Model of Subarachnoid Hemorrhage.
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DOI:
10.3390/diseases11040130
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发表时间:
2023-09-27
期刊:
Diseases (Basel, Switzerland)
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其他
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迟发性脑缺血(DCI)是导致蛛网膜下腔出血(SAH)患者预后不良的重要因素。我们之前已经证明,挥发性麻醉剂如异氟烷、七氟烷和地氟烷对SAH诱导的DCI提供了强有力的保护,但更常用的静脉麻醉剂丙泊酚的影响尚不清楚。本研究旨在探讨异丙酚对蛛网膜下腔出血(SAH)诱导的脑缺血的神经血管保护作用。使用10周龄雄性野生型小鼠进行研究。小鼠进行血管内穿孔SAH或假手术,1小时后通过颈内静脉输注丙泊酚(2 mg/kg/min连续静脉输注)。SAH后3天评估大动脉血管痉挛。在基线时进行神经学结局评估,然后每天进行一次,直至动物处死。统计分析通过单因素ANOVA和双因素重复测量ANOVA进行,然后进行Newman-Keuls多重比较检验,显著性设定为p < 0.05。静脉注射丙泊酚对SAH引起的大动脉血管痉挛或感觉运动神经功能缺损没有任何保护作用。我们的数据表明,异丙酚并没有提供显着的保护对蛛网膜下腔出血诱导的DCI。这些结果与最近的临床研究一致,这些研究表明,麻醉条件反射提供的神经血管保护作用严重依赖于麻醉剂的种类。
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 p < 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.
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