Taiwo Y O, Levine J D
Department of Anatomy, University of California, San Francisco 94143-0724.
Brain Res. 1990 Dec 24;537(1-2):372-4. doi: 10.1016/0006-8993(90)90389-s.
The nonsteroidal anti-inflammatory drugs are presumed to produce their analgesic effects by inhibiting the cyclooxygenase catalyzed metabolism of arachidonic acid to hyperalgesic prostanoids. This study examined the hyperalgesic effect of a range of prostaglandins. We found, employing the rat paw-withdrawal test, that while intradermal injection of the known hyperalgesic prostaglandins, E2 and I2, produced hyperalgesia, other primary metabolites of the cyclooxygenation of arachidonic acid (prostaglandin F2 alpha, prostaglandin D2, thromboxane B2 and 12(S) hydroxyheptadecatrienoic acid) did not produce hyperalgesia. We conclude that prostaglandin E2 and prostaglandin I2 are the main hyperalgesic metabolites of the cyclooxygenase pathway of arachidonic acid.
非甾体抗炎药被认为是通过抑制环氧化酶催化花生四烯酸代谢为痛觉过敏前列腺素而产生镇痛作用的。本研究检测了一系列前列腺素的痛觉过敏作用。我们通过大鼠足趾退缩试验发现，皮内注射已知的痛觉过敏前列腺素E2和I2会产生痛觉过敏，而花生四烯酸环氧化的其他主要代谢产物（前列腺素F2α、前列腺素D2、血栓素B2和12(S)羟基十七碳三烯酸）不会产生痛觉过敏。我们得出结论，前列腺素E2和前列腺素I2是花生四烯酸环氧化酶途径的主要痛觉过敏代谢产物。
