异氟烷通过增加脊髓缺血再灌注损伤中大鼠神经细胞的凋亡、变性从而损害大鼠运动功能的恢复
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Isoflurane Impairs Motor Function Recovery by Increasing Neuroapoptosis and Degeneration During Spinal Ischemia–Reperfusion Injury in Rats
背景与目的
脊髓缺血（SCI）导致接受心血管手术患者不同程度的神经功能缺损。术中神经保护作用对SCI和随后的缺血再灌注损伤仍然有限。异氟烷是大手术中常用的麻醉药物，它的神经保护和神经毒性作用都已被讨论，本研究旨在讨论脊髓缺血大鼠模型中异氟烷对脊髓功能恢复的影响。
方 法
随机给大鼠肠胃外麻醉或异氟烷麻醉（氧气含0％或1.5％v/v）。通过钳闭T5的水平上的胸主动脉来诱导脊髓缺血，并且在25分钟后恢复脊髓灌注。再灌注后48小时独立评估大鼠运动功能。获取大鼠脊髓，分析分子和组织学变化。
结 果
脊髓缺血过程中吸入异氟烷的大鼠在再灌注后12〜48小时的运动评分显著降低。异氟烷增强了血红素加氧酶-1，胶质纤维酸性蛋白，caspase-3蛋白和Iba-1在脊髓中的表达。另外在组织学部分观察到增加的凋亡细胞和轴突损伤。
结 论
我们的研究结果表明，异氟烷在脊髓缺血再灌注损伤中的应用损害了运动功能的恢复，这与神经元凋亡和变性相关。这项研究突出了异氟烷对主动脉手术中缺血脊髓功能恢复的潜在不利影响。
原始文献摘要
Shih-Yuan Fang, MD,Jung-Shun Lee, MD, MSc, Jun-Neng Roan, MD, Yu-Chuan Tsai, MD,and Chen-Fuh Lam, MD, PhD.Isoflurane Impairs Motor Function Recovery by Increasing Neuroapoptosis and Degeneration During Spinal Ischemia–Reperfusion Injury in Rats.Anesth Analg 2017;124:254–61.
BACKGROUND: Spinal cord ischemia (SCI) leads to variable degrees of neurologic deficit in patients undergoing major cardiovascular surgery. The effect of intraoperative neuroprotection against SCI and the subsequent ischemia–reperfusion injury is still limited.Because isoflurane is a commonly used anesthetic agent during major operation, and its neuroprotective and neurotoxicity effects have both been discussed, this study aimed to
investigate the effect of isoflurane on the spinal cord’s functional recovery in a rat model of cord ischemia.
METHODS: Rats were randomly anesthetized by parenteral anesthetic (Zoletil?) and isoflurane (0% and 1.5% v/v in oxygen). Cord ischemia was induced by cross-clamping of thoracic aorta at the level of T5, and cord perfusion was resumed after 25 minutes. The motor function was assessed independently up to 48 hours after reperfusion. Spinal cords were harvested and analyzed for molecular and histologic changes.
RESULTS: The locomotor rating scale was significantly reduced in rats that received isoflurane treatment during SCI at 12 to 48 hours after reperfusion. Isoflurane enhanced the expression of heme oxygenase-1, glial fibrillary acidic protein, cleaved caspase-3, and Iba-1 in the spinal cord. Increased apoptotic cells and the presence of axonal damage were also observed in the histologic sections.
CONCLUSION: Our results demonstrate that the administration of inhaled isoflurane in spinal cord ischemia–reperfusion injury impairs the recovery of motor function. This response isassociated with the neuronal apoptosis and degeneration. This study highlights the potential adverse effect of isoflurane on the functional recovery of ischemic spinal cord during major aortic surgery.
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