S-亚硝基化谷胱甘肽还原酶抑制剂调控心搏骤停-心肺复苏后脑损伤的研究进展

Research progress of S-nitrosoglutathione reductase inhibitors in the regulation of cerebral injury after cardiac arrest-cardiopulmonary resuscitation

心搏骤停(CA)-心肺复苏(CPR)后出现的脑缺血/再灌注损伤(CIRI)是一系列复杂反应的病理生理过程。一氧化氮(NO)在体内是介导细胞信号转导的小分子物质,在缺血/再灌注(I/R)过程中对大脑功能调节有重要作用。S-亚硝基化谷胱甘肽还原酶(GSNOR)抑制剂可控制体内NO的合成与释放,对CIRI具有保护作用。因此,对CA-CPR患者早期给予GSNOR抑制剂可成为改善患者预后的重要治疗手段。近年来国内外就改善CA-CPR后患者的预后进行了大量研究。本文对CA-CPR后大脑损伤的主要机制、NO对I/R损伤的保护作用及机制、NO的体内生成及调节、GSNOR抑制剂对CIRI的保护作用,尤其是对GSNOR抑制剂的研究进展进行综述,以期为进一步研究CA-CPR后CIRI的治疗及大脑保护提供参考。

The cerebral ischemia-reperfusion injury(CIRI)after the cardiac arrest(CA)-cardiopulmonary resuscitation(CPR)was a complex pathophysiology process.Nitric oxide(NO)is a small molecule that mediates cell signal transduction in vivo and plays an important role in the regulation of brain function during ischemia/reperfusion(I/R).S-nitrosoglutathione reductase(GSNOR)inhibitor can regulate the synthesis and release of NO in vivo and has a protective effect on CIRI.Therefore,early administration of GSNOR to CA-CPR patients could be the main treatment method to improve the prognosis of those patients.A large number of studies have been done to improve the prognosis of CA-CPR in recent years.In order to provide reference for further research on the treatment and brain protection of CIRI after CA-CPR,the article reviewed the main mechanisms of brain injury after CA-CPR,the protective effect and mechanism of NO on cerebral I/R injury,the production and regulation of NO,in vivo,and the protective effect of GSNOR inhibitors on CIRI,especially the research progress of GSNOR inhibitors.