Ischemic-preconditioning does not prevent neuromuscular dysfunction after ischemia-reperfusion injury
Ischemic-preconditioning does not prevent neuromuscular dysfunction after ischemia-reperfusion injury
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DOI：
10.1016/j.orthres.2003.10.015
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发表时间：
2004-07-01
影响因子：
2.8
通讯作者：
Pedowitz, RA
中科院分区：
文献类型：
--
作者：
Eastlack, RK;Groppo, ER;Pedowitz, RA
本研究的主要目的是评价缺血预处理（IPC）作为一种改善缺血再灌注（IR）应激对神经肌肉功能的耐受性的手段。第二个目的是分离IR损伤后引起收缩功能障碍的神经肌肉单位内的损伤区域。将28只雄性家兔随机分为4组（假手术组、单纯IPC组、单纯持续缺血组、IPC组和持续缺血组）。IPC方案包括三个循环，10分钟止血带诱导的缺血（125 mmHg），然后再灌注10分钟。采用350 mmHg外压2 h造成持续性缺血。通过腓神经和直接肌肉刺激（有和没有药物神经肌肉接头阻滞），在止血带方案后48小时评估胫骨前肌（TA）的峰值强直张力。接受IPC和持续性缺血联合治疗的动物与仅接受持续性缺血治疗的动物相比，收缩力损失相当。当通过腓神经刺激评估时，止血带诱导的缺血2小时导致TA神经肌肉单位的显著功能障碍（p < 0.0001）。在缺血3小时后，用直接肌肉刺激和神经肌肉接头阻断将TA肌肉与腓神经分离保留肌肉功能。在我们的模型中，这些结果清楚地表明，IPC在我们的模型中对神经或肌肉功能的IR损伤没有提供显著的保护作用。此外，神经或神经肌肉接头损伤，而不是肌肉运输，被确定为主要负责IR相关的肌肉功能障碍。(C)2003骨科研究学会。由爱思唯尔有限公司出版。保留所有权利。
The primary purpose of this study was to evaluate ischemic-preconditioning (IPC) as a means of improving tolerance to ischemia-reperfusion (IR) stress on neuromuscular function. A secondary objective was to isolate the area of injury within the neuromuscular unit responsible for contractile dysfunction after IR injury. Twenty-eight male rabbits were randomly assigned to four groups (sham, IPC only, sustained ischemia only, IPC and sustained ischemia). The IPC protocol consisted of three cycles of 10 min of tourniquet-induced ischemia (125 mmHg) followed by 10 min of reperfusion. Sustained ischemia was induced by 350 mmHg external compression for 2 h. Peak tetanic tension of the tibialis anterior (TA) muscle was evaluated 48 It after the tourniquet protocol by both peroneal nerve and direct muscle stimulation, with and without pharmacologic neuromuscular junction blockade. Animals subjected to combined IPC and sustained ishemia had an equivalent loss of contractile force to those undergoing sustained ischemia alone. Two hours of tourniquet-induced ischemia resulted in marked dysfunction of the TA neuromuscular unit when evaluated by peroneal nerve Stimulation (p < 0.0001). Isolation of the TA muscle from the peroneal nerve with direct muscle stimulation and neuromuscular junction blockade preserved muscle function after 3 h of ischemia. In our model, these results clearly demonstrate that IPC provides no significant protective effect from IR injury to either nerve or Muscle function in Our model. In addition, nerve or neuromuscular junction injury, rather than muscle carriage, is identified as primarily responsible for IR-related muscle dysfunction. (C) 2003 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved.