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非甾体抗炎药对紫外线诱导的皮肤炎症影响的重新评估。

Re-evaluation of the effect of non-steroidal anti-inflammatory agents on u.v.-induced cutaneous inflammation.

作者信息

Woodward D F, Raval P, Pipkin M A, Owen D A

出版信息

Agents Actions. 1981 Dec;11(6-7):711-7. doi: 10.1007/BF01978794.

Abstract

The effect of non-steroidal anti-inflammatory agents on u.v. radiation-induced cutaneous inflammation has been re-evaluated using a model which permits simultaneous and quantitative measurement of vasodilatation, vascular permeability and oedema formation throughout the entire time course of the inflammatory reaction. Indomethacin and phenylbutazone produced a substantial reduction in u.v. erythema during the initial stages but subsequently were far less effective, although small, significant reductions were obtained. Attempts to reverse an established inflammatory response to u.v. injury also yielded small, significant reductions in erythema but vascular permeability remained unaffected. In addition, it was found that arachidonic acid and prostaglandin E2 selectively produced vasodilatation: the vasodilator response to arachidonic acid, but not prostaglandin E2, was greatly reduced by indomethacin. It is suggested that cyclo-oxygenase derived arachidonic acid metabolites play an important role in mediating u.v. erythema only during the initial period.

摘要

使用一种能够在炎症反应的整个时间进程中同步且定量地测量血管舒张、血管通透性和水肿形成的模型,对非甾体抗炎药对紫外线辐射诱导的皮肤炎症的影响进行了重新评估。吲哚美辛和保泰松在炎症反应初始阶段能使紫外线红斑显著减轻,但随后效果就差得多了,尽管仍能获得小幅度但显著的减轻。试图逆转已确立的对紫外线损伤的炎症反应,也能使红斑有小幅度但显著的减轻,但血管通透性未受影响。此外,还发现花生四烯酸和前列腺素E2可选择性地引起血管舒张:吲哚美辛可大大降低对花生四烯酸的血管舒张反应,但对前列腺素E2的反应无此作用。提示环氧化酶衍生的花生四烯酸代谢产物仅在初始阶段在介导紫外线红斑中起重要作用。

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