肾缺血再灌注损伤是导致急性肾小管坏死和肾移植失败的重要因素,如何减轻和预防肾脏缺血再灌注损伤,一直是保护急性肾损伤研究的主要内容.肾缺血再灌注损伤的发病机制非常复杂,研究资料表明,内皮素1、一氧化氮和肾素-血管紧张素系统(RAS)中的主要活性物质如血管紧张素Ⅱ和血管紧张素(1-7)等血管活性物质可能在肾缺血再灌注损伤中起重要作用,并参与其发生、发展.%The key factor of acute tubule necrosis and the failure of renal transplant is renal ischemia reperfusion injury (RIRI) , how to relieve or prevent it is always the key issues of protection of renal injury. The pathological mechanism of RIRI is very complicated, the data of current research demonstrate that some vaso-active substances, such as ET-1, NO, the renin-angiotensin system( RAS) of angiotensin II or Ang( 1-7 ) play an important role in RIRI, and take part in the occurrence and development of renal injury.
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