Department of Anatomy and Neurobiology, Virginia Commonwealth University Medical Center, Richmond, VA 23298, USA.
J Neurotrauma. 2011 Jul;28(7):1209-18. doi: 10.1089/neu.2011.1852.
Following traumatic brain injury (TBI), inhibition of reactive oxygen species and/or calcineurin can exert axonal and vascular protection. This protection proves optimal when these strategies are used early post-injury. Recent work has shown that the combination of delayed drug administration and delayed hypothermia extends this protection. Here we revisit this issue in TBI using the nitroxide antioxidant Tempol, or the immunophilin ligand FK506, together with delayed hypothermia, to determine their effects upon cerebral vascular reactivity and axonal damage. Animals were subjected to TBI and treated with Tempol at 30 or 90 min post-injury, or 90 min post-injury with concomitant mild hypothermia (33°C). Another group of animals were treated in the same fashion with the exception that they received FK506. Cranial windows were placed to assess vascular reactivity over 6 h post-injury, when the animals were assessed for traumatically induced axonal damage. Vasoreactivity was preserved by early Tempol administration; however, this benefit declined with time. The coupling of hypothermia and delayed Tempol, however, exerted significant vascular protection. The use of early and delayed FK506 provided significant vascular protection which was not augmented by hypothermia. The early administration of Tempol provided dramatic axonal protection that was not enhanced with hypothermia. Early and delayed FK506 provided significant axonal protection, although this protection was not enhanced by delayed hypothermia. The current investigation supports the premise that Tempol coupled with hypothermia extends its benefits. While FK506 proved efficacious with early and delayed administration, it did not provide either increased vascular or axonal benefit with hypothermia. These studies illustrate the potential benefits of Tempol coupled to delayed hypothermia. However, these findings do not transfer to the use of FK506, which in previous studies proved beneficial when coupled with hypothermia. These divergent results may be a reflection of the different animal models used and/or their associated injury severity.
颅脑损伤(TBI)后,抑制活性氧和/或钙调神经磷酸酶可发挥轴突和血管保护作用。当这些策略在损伤后早期使用时,这种保护作用最佳。最近的研究表明,延迟药物治疗和延迟低温相结合可延长这种保护作用。在这里,我们使用抗氧化剂氮氧化物 Tempol 或免疫亲和配体 FK506 与延迟低温一起在 TBI 中重新研究这个问题,以确定它们对脑血管反应性和轴突损伤的影响。动物接受 TBI 并在损伤后 30 或 90 分钟或损伤后 90 分钟同时接受轻度低温(33°C)进行 Tempol 治疗。另一组动物以相同的方式治疗,但接受 FK506。在损伤后 6 小时放置颅窗以评估血管反应性,此时评估创伤性诱导的轴突损伤。早期 Tempol 给药可保持血管反应性;然而,这种益处随着时间的推移而下降。低温和延迟 Tempol 的联合使用可发挥显著的血管保护作用。早期和延迟 FK506 的使用提供了显著的血管保护作用,而低温并没有增强这种保护作用。早期 Tempol 的给药提供了显著的轴突保护作用,而低温并没有增强这种保护作用。早期和延迟 FK506 提供了显著的轴突保护作用,尽管低温没有增强这种保护作用。目前的研究支持这样的前提,即 Tempol 与低温结合可延长其益处。虽然 FK506 早期和延迟给药均有效,但与低温结合并不能增加血管或轴突获益。这些研究说明了 Tempol 与延迟低温相结合的潜在益处。然而,这些发现不适用于 FK506 的使用,FK506 在以前的研究中与低温结合证明是有益的。这些不同的结果可能是由于使用了不同的动物模型及其相关的损伤严重程度所致。