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内耳缺血再灌注损伤机制的研究进展
引用本文:许险艳,郑鸣. 内耳缺血再灌注损伤机制的研究进展[J]. 解剖与临床, 2009, 14(6): 446-449. DOI: 10.3969/j.issn.1673-7163.2009.06.021
作者姓名:许险艳  郑鸣
作者单位:福建医科大学解剖教研室,福建福州,350108
摘    要:目的:探讨内耳缺血再灌注损伤的发病机制,为临床治疗提供理论依据。方法:查阅近年国内外有关内耳缺血再灌注损伤发病机制的相关文献,并做进一步综合分析。结果:内耳缺血再灌注损伤的发病机制是一个复杂的病理生理过程,这个级联反应包括许多环节,如能量障碍、细胞酸中毒、兴奋性氨基酸释放增加、钙超载、自由基生成、炎性因子释放、线粒体损伤等。结论:内耳缺血再灌注损伤机制是多方面因素综合作用的结果,早期发现、全面干预是治疗的基本原则。

关 键 词:内耳  缺血再灌注  发病机制

Advance in Pathogenesy of Ischemical Reperfusion Injury in Inner Ear
XU Xian-Yan,Zheng Ming. Advance in Pathogenesy of Ischemical Reperfusion Injury in Inner Ear[J]. Anatomy and Clinics, 2009, 14(6): 446-449. DOI: 10.3969/j.issn.1673-7163.2009.06.021
Authors:XU Xian-Yan  Zheng Ming
Affiliation:(Department of Anatomy and Histo-embryology, Fujian Medical University, Fuzhou, Fujian 350004, China)
Abstract:Objective:To review the literatures about the development of pathogenesy of ischemical reperfusion injury in inner ear, in order to provide theory evidence for clinical therapy. Methods : The related biomedical research materials at home and abroad were consulted and analyzed. Results:Ischemical reperfusion injury of inner ear is a complex pathophysiological process, there are many links in this cascade reaction, including disturbance of energy, cellular acidosis, increased releasing of excitatory amino acid, calcium overload, production of free radical, releasing of inflammatory cytokines and impairment of mitochondrion. Conclusions: Multi-factors attribute to the development of ischemcial reperfusion injury of inner ear that detecting in early phase and overall intervention are the basic principles of therapy.
Keywords:Inner ear  Ischemical reperfusion injury  Pathogenesy
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