阿司匹林对沙土鼠全脑缺血-再灌注后脑内一氧化氮合酶及一氧化氮的影响

目的观察阿司匹林对沙土鼠全脑缺血-再灌注后的脑保护作用及其与脑内一氧化氮合酶及一氧化氮水平变化的关系。方法采用夹闭双侧颈总动脉的方法,制备沙土鼠短暂性全脑缺血-再灌注模型。27只健康雄性蒙古沙土鼠随机分为假手术组、脑缺血-再灌注组和阿司匹林治疗组,观察缺血7min再灌注24h后沙土鼠脑组织的病理学改变,以及一氧化氮合酶与一氧化氮水平的变化。结果病理学检查结果显示,沙土鼠脑缺血7min再灌注24h后海马CA1区缺血性损害明显,脑组织内一氧化氮合酶及一氧化氮水平显著升高(P<0.01);与脑缺血-再灌注组相比,阿司匹林治疗组沙土鼠的病理损害较轻,一氧化氮合酶与一氧化氮水平明显下降(P<0.01)。结论阿司匹林可显著减轻脑缺血-再灌注后的脑损伤,其作用机制可能与抑制一氧化氮合酶与一氧化氮水平上升有关。

Effect of aspirin on intracerebral levels of NOS and NO after reperfusion in cerebral ischemic gerbils

Objective To study the effects of aspirin on brain protection and intracerebral level of NOS and NO after cerebral ischemia reperfusion in gerbil s. Methods The model of transient brain ischemia-reperfusion was established in gerbils by bilateral carotid artery clamping. Twenty-seven healthy gerbils wer e randomly divided into sham operation group, ischemia-reperfusion group and asp irin treated group. The pathological changes and levels of NOS and NO in brain tissue with ischemia for 7 min and then reperfusion for 24 hours were studied. Results Pathological examination showed that in CA1 area of hippocampus in gerbi ls after 7 min ischemia and reperfusion for 24 hours, the ischemic injury was ob vious and the levels of NOS and NO in cerebral tissue were significantly increas ed (P < 0.01). Compared with ischemia-reperfusion group, the less pathological changes of gerblis in aspirin group were found and levels of NOS and NO decrease d obviously (P < 0.01). Conclusion It demonstrates that aspirin can ameliorate brain injury after ischemia-reperfusion, its mechanism may be associated with th e inhibition for increasing levels of NOS and NO.