Free radical mediated damage in skeletal muscle.

T Lindsay, A Romaschin, P M Walker
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Abstract

Skeletal muscle subjected to prolonged ischemia will develop significant injury, however it can withstand periods of ischemia that would be irreversible in other tissues such as brain and heart. Reperfusion injury has been measured and suggested to occur secondary to oxygen free radicals. The increases in vascular permeability and resistance following ischemia/reperfusion can be blunted using free radical scavengers. Also skeletal muscle necrosis can be reduced if these scavengers are provided in high concentration during reperfusion. Recently increases in hydroxy-conjugated dienes, a marker of lipid peroxidation, have been found in reperfused skeletal muscle, providing chemical evidence for free radical injury during reperfusion. These studies have provided some insight into ischemia/reperfusion injury in skeletal muscle, but more investigations are required to detail the mechanisms involved in this injury.

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自由基介导的骨骼肌损伤。
骨骼肌经受长时间缺血会产生明显的损伤,但它可以承受其他组织如大脑和心脏不可逆的缺血期。再灌注损伤已被测量,并提示继发于氧自由基。缺血/再灌注后血管通透性和阻力的增加可以用自由基清除剂来减弱。此外,如果在再灌注时提供高浓度的这些清除剂,骨骼肌坏死也可以减少。最近,在再灌注骨骼肌中发现了脂质过氧化标志物羟基共轭二烯的增加,这为再灌注时自由基损伤提供了化学证据。这些研究为骨骼肌缺血/再灌注损伤提供了一些见解,但需要更多的研究来详细说明这种损伤的机制。
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