Limb Remote Ischemic Preconditioning Protects the Spinal Cord from Ischemia-Reperfusion Injury A Newly Identified Nonneuronal but Reactive Oxygen Species-dependent Pathway
Limb Remote Ischemic Preconditioning Protects the Spinal Cord from Ischemia-Reperfusion Injury A Newly Identified Nonneuronal but Reactive Oxygen Species-dependent Pathway
复制标题
肢体远程缺血预处理保护脊髓免受缺血再灌注损伤：一种新发现的非神经元但活性氧依赖的途径
DOI：
10.1097/aln.0b013e3181d0486d
复制
发表时间：
2010-04-01
期刊：
影响因子：
8.8
通讯作者：
Xiong, Lize
中科院分区：
文献类型：
--
作者：
Dong, Hai-Long;Zhang, Yi;Xiong, Lize
背景资料：肢体远端缺血预处理（limb remote ischemic preconditioning，RIPC）是否能诱导脊髓缺血耐受，RIPC对脊髓的保护作用机制尚待进一步研究。实验一采用主动脉阻断法造成脊髓缺血20分钟。缺血前30 min，对家兔进行假手术或双侧股动脉闭塞（缺血10 min/再灌注10 min，2个周期）的RIPC。二甲基硫脲（500毫克/公斤，静脉注射），羟基自由基清除剂，或车辆前1小时RIPC。抗氧化酶活性测定沿着脊髓组织学和神经功能。实验2：兔脊髓缺血，加或不加RIPC。结果：RIPC可改善神经功能，减轻组织学损害。这与内源性抗氧化活性增加有关。二甲基硫脲可抑制RIPC的保护作用。与此相反，有六烃季铵对RIPC的保护作用没有影响。结论：初始氧化应激作为触发上调抗氧化酶活性，而不是神经通路，并在肢体RIPC对脊髓缺血耐受的形成中起着重要作用。
Background: It remains to be established whether spinal cord ischemic tolerance can be induced by limb remote ischemic preconditioning (RIPC), and the mechanisms underlying the neuroprotective effects of RIPC on the spinal cord need to be clarified.Methods: Spinal cord ischemia was studied in New Zealand White rabbits. In experiment 1, all rabbits were subjected to 20-min spinal cord ischemia by aortic occlusion. Thirty minutes before ischemia, rabbits were subjected to sham intervention or RIPC achieved by bilateral femoral artery occlusion (10 min ischemia/10 min reperfusion, two cycles). Dimethylthiourea (500 mg/kg, intravenously), a hydroxyl radical scavenger, or vehicle was given 1 h before RIPC. Antioxidant enzyme activity was measured along with spinal cord histology and neurologic function. In experiment 2, rabbits were subjected to spinal cord ischemia, with or without RIPC. In addition, rabbits were pretreated with various doses of hexamethonium.Results: RIPC improved neurologic function and reduced histologic damage. This was associated with increased endogenous antioxidant activity. Dimethylthiourea inhibited the protective effects of RIPC. In contrast, there was no effect of hexamethonium on the protective effect of RIPC.Conclusions: An initial oxidative stress acts as a trigger to upregulate antioxidant enzyme activity, rather than the neural pathway, and plays an important role in the formation of the tolerance against spinal cord ischemia by limb RIPC.