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为了探讨腺苷和一氧化氮（ｎｉｔｒｉｃｏｘｉｄｅ，ＮＯ）在缺血再灌注损伤中的作用及二者间的关系，我们在四血管结扎大鼠缺血再灌注模型上，观察了缺血再灌注后脑组织中ＮＯ含量的变化及腺苷Ａｌ受体激动剂ＣＨＡ（ｃｙｃｌｏｈｅｘｙｌａｄｅｎｏｓｉｎｅ）的影响。结果显示：大鼠全脑缺血３０分钟，再灌注１５分钟后脑组织中的ＮＯ含量提高，提示ＮＯ参与了缺血再灌注损伤的病理过程。ＣＨＡ可以降低缺血再灌注时ＮＯ的含量．提示腺苷对脑缺血再灌注时的保护作用可能与抑制缺血时脑组织中ＮＯ的过度增高有关。
In order to explore the role of adenosine and nitric oxide (NO) in the process of ischemia-reperfusion injury and their relationship, we observed the effect of ischemia-reperfusion on the model of ischemia- NO content in tissues and the effect of adenosine Al receptor agonist CHA (cyclohexyladenosine). The results showed that the content of NO in brain increased 30 minutes after global cerebral ischemia and 15 minutes after reperfusion, suggesting that NO participates in the pathological process of ischemia-reperfusion injury. CHA can reduce the content of NO during ischemia-reperfusion. These results suggest that the protective effect of adenosine on cerebral ischemia-reperfusion may be related to the inhibition of NO excessive increase of brain tissue during ischemia.