MODULATION OF ACUTE-INFLAMMATION BY ENDOGENOUS NITRIC-OXIDE
MODULATION OF ACUTE-INFLAMMATION BY ENDOGENOUS NITRIC-OXIDE
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DOI：
10.1016/0014-2999(92)90526-a
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发表时间：
1992-02-11
影响因子：
5
通讯作者：
DIROSA, M
中科院分区：
文献类型：
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作者：
IALENTI, A;IANARO, A;DIROSA, M
用两种NO合成酶抑制剂（N（G）-硝基-L-精氨酸甲酯（L-NAME）和N（G）-单甲基-L-精氨酸（L-NMMA））以及L-或D-精氨酸研究了内源性一氧化氮（NO）在急性炎症中的作用。研究了测试化合物对角叉菜胶诱导的大鼠皮肤血管通透性增加以及对葡聚糖和角叉菜胶诱导的爪水肿的影响。L-NAME和L-NMMA剂量依赖性地抑制血管通透性的增加和水肿形成。L-而不是D-精氨酸增加这些炎症反应，并逆转L-NAME和L-NMMA的抑制作用。在地塞米松处理的大鼠中，L-精氨酸增强了右旋糖酐诱导的水肿和角叉菜胶诱导的水肿的早期阶段，但没有修改地塞米松对角叉菜胶诱导的水肿的晚期阶段的抑制。这些结果表明，内源性NO在急性炎症部位释放并调节水肿形成。根据时间进程或炎症的类型，NO可以主要由组成型或诱导型NO合酶产生。
The role of endogenous nitric oxide (NO) in acute inflammation was investigated using two inhibitors of NO synthase (N(G)-nitro-L-arginine methyl ester(L-NAME) and N(G)-monomethyl-L-arginine (L-NMMA)) as well as L- or D-arginine. The effect of test compounds was studied on the carrageenin-induced increase in vascular permeability in rat skin and in dextran- and carrageenin-induced paw oedema. Both L-NAME and L-NMMA dose dependently inhibited the increase in vascular permeability and oedema formation. L- but not D-arginine increased these inflammatory responses and reversed the inhibitory effects of L-NAME and L-NMMA. In dexamethasone-treated rats L-arginine enhanced the dextran-induced oedema and the early phase of carrageenin-induced oedema but did not modify the inhibition by dexamethasone of the late phase of carrageenin-induced oedema. These results suggest that endogenous NO is released at the site of acute inflammation and modulates oedema formation. Depending on the time course or on the type of inflammation, NO may be predominantly generated by the constitutive or by the inducible NO synthase.