Remote organ ischemic preconditioning protect brain from ischemic damage following asphyxial cardiac arrest

Remote organ ischemic preconditioning protect brain from ischemic damage following asphyxial cardiac arrest
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DOI:
10.1016/j.neulet.2006.05.037
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发表时间:
2006-08-14
影响因子:
2.5
通讯作者:
Perez-Pinzon, Miguel A.
Perez-Pinzon, Miguel A.
中科院分区:
医学4区
文献类型:
--
作者:
Dave, Kunjan R.;Saul, Isabel;Perez-Pinzon, Miguel A.

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缺血预处理(IPC)是一种现象,通过用短时间的亚致死/轻度缺血性损伤来预处理该器官,器官对致命性缺血性损伤产生适应性瞬时抵抗。除了 IPC 之外,最近的研究报告称,各个器官的短暂亚致死性缺血和再灌注也可以诱导另一个器官的缺血耐受。这种现象被称为远程缺血预处理(RPC)。在本研究中,我们测试了以下假设:在窒息性心脏骤停 (ACA) 大鼠模型中,RPC 和 IPC 可以诱导大脑对缺血的耐受性。通过使用止尿带收紧双后肢的上三分之二15或30分钟来诱导RPC,通过收紧双侧颈动脉结扎线2分钟来诱导IPC。 RPC 或 IPC 后 48 It 诱导 8 分钟的 ACA。复苏7天后,取出大脑并检查组织病理学变化。在 CA1 海马区,心脏骤停大鼠的正常神经元数量比对照组低 63%。 15 min RPC、30 min RPC 和 IPC 组的正常神经元数量分别比 ACA 组高 54%、70% 和 67%。这项研究表明 RPC 和 IPC 能够在 ACA 大鼠模型中提供神经保护。除了直接应用 RPC 或 IPC 范式外,探索 RPC 和 IPC 所观察到的神经保护机制也可能为 CA 患者带来可能的治疗方法。 (c) 2006 Elsevier Ireland Ltd. 保留所有权利。
Ischemic preconditioning (IPC) is a phenomenon whereby an organ's adaptive transient resistance to a lethal ischemic insult occurs by preconditioning this organ with a sub-lethal/mild ischemic insult of short duration. Besides IPC, recent studies reported that a short sub-lethal ischemia and reperfusion in various organs can induce ischemic tolerance in another organ as well. This phenomenon is known as remote ischemic preconditioning (RPC). In the present study we tested the hypothesis that tolerance for ischemia can be induced in brain by RPC and IPC in a rat model of asphyxial cardiac arrest (ACA). RPC was induced by tightening the upper two-thirds of both hind limbs using a toumiquet for 15 or 30 min and IPC was induced by tightening bilateral carotid artery ligatures for 2 min. Eight minutes of ACA was induced 48 It after RPC or IPC. After 7 day of resuscitation, brains were extracted and examined for histopathological changes. In CA1 hippocampus, the number of normal neurons was 63% lower in cardiac-arrested rats as compared to the control group. The number of normal neurons in the 15 min RPC, 30 min RPC, and IPC groups was higher than the ACA group by 54, 70, and 67%, respectively. This study demonstrates that RPC and IPC are able to provide neuroprotection in a rat model of ACA. Besides direct application of RPC or IPC paradigms, the exploration of the mechanisms of observed neuroprotection by RPC and IPC may also lead to a possible therapy for CA patients. (c) 2006 Elsevier Ireland Ltd. All rights reserved.