Pang C Y
Division of Surgical Research, Hospital for Sick Children, Toronto, Ontario, Canada.
J Reconstr Microsurg. 1990 Jan;6(1):77-83. doi: 10.1055/s-2007-1006807.
Experimental evidence available currently indicates that injury to the muscle during reperfusion is most likely mediated by oxygen-derived free radicals (oxyradicals). The major oxyradical generating system in the skeletal muscle has yet to be identified so that an appropriate oxyradical-generating inhibitor and/or scavenger can be selected for the prevention of ischemia-induced reperfusion injury to the skeletal muscle. In addition, apart from generating oxyradicals, the activated leukocytes, platelets, and vascular endothelial cells are also known to synthesize and release vasoconstrictive substances and/or chemoattractants for leukocytes. The role of these locally released chemical substances in the pathogenesis of ischemia-induced reperfusion injury in muscle flaps has yet to be elucidated. The pathophysiology of ischemia-induced reperfusion injury to the skeletal muscle in muscle flaps is reviewed.
目前可得的实验证据表明，再灌注期间肌肉损伤最有可能由氧衍生自由基（氧自由基）介导。骨骼肌中主要的氧自由基生成系统尚未确定，因此无法选择合适的氧自由基生成抑制剂和/或清除剂来预防骨骼肌缺血诱导的再灌注损伤。此外，除了生成氧自由基外，活化的白细胞、血小板和血管内皮细胞还已知会合成并释放血管收缩物质和/或白细胞趋化剂。这些局部释放的化学物质在肌皮瓣缺血诱导的再灌注损伤发病机制中的作用尚未阐明。本文综述了肌皮瓣中骨骼肌缺血诱导的再灌注损伤的病理生理学。
