Linked Life Data

7525183

Source:http://linkedlifedata.com/resource/pubmed/id/7525183

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1994-12-13
pubmed:abstractText
The traditional classification of nonsteroidal anti-inflammatory drugs (NSAIDs) as exclusively 'peripherally acting' agents is no longer valid. For many of these agents there is a growing body of evidence in favour of an additional central mechanism for their anti-inflammatory and analgesic effects. This view is further supported by the recent discovery that a substantial component of the hyperalgesia and allodynia that characterise postinjury hypersensitivity occurs in the CNS, notably the spinal dorsal horn. An important corollary is that inhibition of central nociceptive processing may represent an important analgesic mode of action for those NSAIDs that are effective in the management of pain after tissue injury. Historically, attempts to group this heterogeneous class of compounds into a single entity are largely derived from the observation that the majority of clinically useful NSAIDs are weak organic acids (pKa 3 to 5), bind extensively to plasma albumin (= 99%), and inhibit (to varying degrees) prostaglandin synthesis. However, the significance of these various unifying features is becoming increasingly obscure. While inhibition of prostaglandin synthesis apparently remains an important analgesic mode of action for NSAIDs both in the periphery and the CNS, other mechanisms should be considered. Some NSAIDs, in addition to their effects on prostaglandin synthesis, also affect the synthesis and activity of other neuroactive substances believed to have key roles in processing nociceptive input within the dorsal horn. It has been argued that these other actions, in conjunction with inhibition of prostaglandin synthesis, may synergistically augment the effects of NSAIDs on spinal nociceptive processing. Despite much effort, it remains a formidable task to assess the significance of these differential mechanisms upon clinical pain states. In the meantime, however, it may be possible, on the basis of in vivo studies, to evaluate the impact of putative spinal analgesic mechanisms that are unrelated to inhibition of prostaglandin synthesis. This approach has recently been extended to include the identification of pharmacokinetic and clinical correlates of these derived in vivo parameters, and in this way attempt to demonstrate clinical relevance.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0012-6667
pubmed:author
pubmed:issnType
Print
pubmed:volume
47 Suppl 5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
28-45; discussion 46-7
pubmed:dateRevised
2004-11-17
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
The spinal actions of nonsteroidal anti-inflammatory drugs and the dissociation between their anti-inflammatory and analgesic effects.
pubmed:affiliation
Drug Research Group, McCormack Ltd., Bedfordshire, England.
pubmed:publicationType
Journal Article, Review