Effects of cyclooxygenase products of arachidonic acid metabolism on cutaneous nociceptive threshold in the rat.

Abstract:

: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.

journal_name

Brain Res

journal_title

Brain research

authors

Taiwo YO,Levine JD

doi

10.1016/0006-8993(90)90389-s

subject

Has Abstract

pub_date

1990-12-24 00:00:00

pages

372-4

issue

1-2

eissn

0006-8993

issn

1872-6240

pii

0006-8993(90)90389-S

journal_volume

537

pub_type

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