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The study on pathological mechanism and solution method for spinal cord ischemia reperfusion injury

机译:脊髓缺血再灌注损伤的病理机制及解决方法的研究

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OBJECTIVE: We aimed at investigating the pathological mechanism changing of injury during reperfusion injury, reperfusion time correlation and compliance, finding the blood supply and improving the secondary damage. MATERIALS AND METHODS: A total of 180 patients who underwent a surgical procedure and that received normal saline intraperitoneally immediately after the patients’ aortic occlusions were investigated. Patients were divided in three groups. Experimental conditions and programs were designed for various approaches. RESULTS: Thirty min after the onset of ischemia, we found a decrease in the local blood flow in the lumbar spinal cord, almost -77.48% of the baseline, which was reversed partially by initial reperfusion, even exceeding the baseline level. However, 1 hour after reperfusion, the blood flow was again decreased to the level below the baseline, followed by a decline to 207.13% ± 38.25 PU for 3 h without any recovery. Attenuating this secondary damage with neuroprotective strategies requires an understanding of these pathophysiologic processes. CONCLUSIONS: This study showed the pathological mechanism changes during reperfusion injury and reperfusion time correlation and compliance, and analyzed some of the important pathophysiologic processes involved in secondary damage after spinal cord injury. Moreover, our research discusses a number of pharmacologic therapies that have either been studied or have future potential for this devastating injury.
机译:目的:研究再灌注损伤过程中损伤的病理机制变化,再灌注时间相关性和依从性,寻找供血情况,改善继发性损伤。材料与方法:共调查了180例行外科手术并在主动脉闭塞后立即腹膜内接受生理盐水的患者。将患者分为三组。针对各种方法设计了实验条件和程序。结果:缺血发作后三十分钟,我们发现腰椎局部血流减少,几乎是基线的-77.48%,最初的再灌注可部分逆转,甚至超过基线水平。但是,再灌注后1小时,血流量再次下降至基线以下水平,随后3h降至207.13%±38.25 PU,无任何恢复。用神经保护策略减轻这种继发性损伤需要了解这些病理生理过程。结论:本研究显示了再灌注损伤期间的病理机制变化以及再灌注时间的相关性和顺应性,并分析了与脊髓损伤后继发性损伤有关的一些重要病理生理过程。此外,我们的研究讨论了许多药物疗法,这些药物疗法已被研究或可能具有毁灭性伤害的潜力。

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