Department of Physiology, Spinal Cord and Brain Injury Research Center, College of Medicine, University of Kentucky, Lexington, Kentucky, USA.
Department of Psychology, University of Kentucky, Lexington, Kentucky, USA.
J Neurotrauma. 2023 Dec;40(23-24):2541-2551. doi: 10.1089/neu.2023.0077. Epub 2023 Jul 21.
Approximately one in three traumatic spinal cord injuries (SCIs) occurs during or shortly after the consumption of alcohol. A small number of retrospective clinical studies report variable effects of alcohol intoxication on mortality, neurological recovery, and complications after SCI. Some of these studies demonstrate a protective effect of alcohol intoxication on SCI outcomes, whereas others show an increased complication risk. Pre-clinical studies in rat, ferret, and feline SCI models report a detrimental effect of ethanol intoxication on hemorrhage, motor recovery, and biochemical markers of tissue injury. However, no studies to date have investigated the neuropathological consequences of ethanol intoxication at the time of SCI or the reciprocal effect of SCI on ethanol metabolism. Therefore, we combined a pre-clinical mouse model of acute ethanol intoxication and experimental vertebral level T9 contusion SCI to investigate their interactive effects in female mice. We first investigated the effect of SCI on ethanol metabolism and found that T9 SCI does not alter ethanol metabolism. However, we did find that isoflurane anesthesia significantly slowed ethanol metabolism independent of SCI. We also determined how acute ethanol intoxication at the time of SCI alters locomotor recovery and lesion pathology. Using the Basso Mouse Scale (BMS) and CatWalk XT Gait Analysis System, we assessed locomotor recovery for 6 weeks after injury and observed that acute ethanol intoxication at the time of injury did not alter locomotor recovery. We also found no effect of ethanol intoxication on heat hyperalgesia development. There was, however, a detrimental effect of ethanol on tissue sparing after SCI. Therefore, we conclude that acute alcohol intoxication at the time of injury may contribute to the neuropathological consequences of SCI.
大约三分之一的外伤性脊髓损伤 (SCI) 发生在饮酒期间或之后不久。少数回顾性临床研究报告了酒精中毒对死亡率、神经恢复和 SCI 后并发症的可变影响。其中一些研究表明酒精中毒对 SCI 结果有保护作用，而另一些研究则表明并发症风险增加。大鼠、雪貂和猫科动物 SCI 模型的临床前研究报告称，乙醇中毒对出血、运动恢复和组织损伤的生化标志物有不利影响。然而，迄今为止，没有研究调查过 SCI 时乙醇中毒的神经病理学后果或 SCI 对乙醇代谢的反作用。因此，我们结合了急性乙醇中毒的临床前小鼠模型和实验性 T9 椎体挫伤 SCI，以研究它们在雌性小鼠中的相互作用。我们首先研究了 SCI 对乙醇代谢的影响，发现 T9 SCI 不会改变乙醇代谢。然而，我们确实发现异氟烷麻醉会显著减缓乙醇代谢，而与 SCI 无关。我们还确定了 SCI 时急性乙醇中毒如何改变运动恢复和病变病理学。我们使用 Basso 小鼠量表 (BMS) 和 CatWalk XT 步态分析系统评估了损伤后 6 周的运动恢复情况，发现损伤时急性乙醇中毒并未改变运动恢复。我们还发现乙醇中毒对热痛觉过敏的发展没有影响。然而，乙醇对 SCI 后组织保存有不利影响。因此，我们得出结论，损伤时急性酒精中毒可能导致 SCI 的神经病理学后果。
