摘要
目的:通过观察长托宁对全脑缺血再灌注大鼠肺内一氧化氮合酶(NOS)活性的影响,探讨长托宁的肺保护作用及其机制。方法:按改良的Pulsinelli方法建立全脑缺血再灌注模型,分别观察假手术组(A组)、缺血再灌注组(B组)和长托宁治疗组(C组)各时间点(2、12、24、48h)肺组织病理学改变并测定其组织NOS活性。结果:①A组未见组织病理学改变,B组均出现组织病理学损伤,以12h时最严重,C组明显改善;②B组总NOS活性在2、12、24h比A组高,以12h时升高最显著,其中在2h时以结构型(cNOS)升高为主;在12h时以诱导型(iNOS)升高为主,且24h时仍升高,48h时基本接近A组水平;③与B组相比,C组cNOS活性在2h时上升更为显著,iNOS在12h及24h时明显下降。结论:①在全脑缺血再灌注时的不同阶段存在不同程度肺损伤;②在脑缺血再灌注不同阶段肺组织中不同类型NOS活性不同,发挥不同作用,长托宁可以调节肺组织不同类型NOS活性,对抗肺组织损伤。
Objective:To explore the protective effects of Penehyclidine on lung injury of rats after cerebral ischemia reperfusion based on the activities of NOS.Methods:The cerebral ischemia reperfusion models were established by Pulsinelli's.Pathologic changes of the lung tissue and activities of NOS were observed at four different times in sham operation group (group A),ischemia-reperfusion group (group B) and treatment group (group C).Results:① There were no pathologic changes in group A,but the changes were obviously observed in group B especially at 12h and were significantly improved in group C.② The activities of total NOS were increased at 2 h,12 h and 24 h in group B compared with those in group A,and they were increased significantly at 12 h.The activities of cNOS and iNOS were increased significantly at 2 h and 12 h respectively.③The activities of cNOS increased much higher at 2 h in group C compared with those in group B,but iNOS were significantly decreased at 12 h and 24 h.Conclusions:Various types NOS play different roles in pulmonary injury after brain ischemia-reperfusion in the different stages in rats.Penehyclidine can improve the damages through modulating the activities of different types of NOS.
出处
《内科急危重症杂志》
2010年第5期249-251,271,共4页
Journal of Critical Care In Internal Medicine
关键词
一氧化氮合酶
脑缺血再灌注
肺损伤
盐酸戊乙奎醚
Nitric oxide synthase Brain ischemia reperfusion Lung injury Penehyclidine hydrochloride