EFFECTS OF CYCLOOXYGENASE PRODUCTS OF ARACHIDONIC-ACID METABOLISM ON CUTANEOUS NOCICEPTIVE THRESHOLD IN THE RAT

被引：54

作者：

TAIWO, YO

LEVINE, JD

机构：

[1] UNIV CALIF SAN FRANCISCO,DEPT MED,U-426,BOX 0724,SAN FRANCISCO,CA 94143

[2] UNIV CALIF SAN FRANCISCO,DEPT ANAT,SAN FRANCISCO,CA 94143

[3] UNIV CALIF SAN FRANCISCO,DEPT ORAL SURG,SAN FRANCISCO,CA 94143

[4] UNIV CALIF SAN FRANCISCO,DIV NEUROSCI,SAN FRANCISCO,CA 94143

来源：

BRAIN RESEARCH | 1990年 / 537卷 / 1-2期

关键词：

HYPERALGESIA; PAIN; PROSTAGLANDIN; CUTANEOUS; PRIMARY AFFERENT NOCICEPTOR;

D O I：

10.1016/0006-8993(90)90389-S

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

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 the 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.

引用

页码：372 / 374

页数：3

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