Friday, April 13, 2012

Inflammatory pain & NSAIDs

Inflammation causes release of many different cytokines & growth factors.

Stimuli in the inflamed area that would normally cause only minor pain produce an exaggerated response (hyperalgesia) and normally innocuous stimuli such as touch cause pain (allodynia)

Many of the cytokines and growth factors facilitate perception and transmission in cutaneous areas as well as in the dorsal horn.

Prostaglandins induce hyperalgesia by affecting the transducing property of free nerve endings.

Prostaglandins and other inflammatory molecules facilitate activation of tetrodoxin resistant Na+ channels in the dorsal root ganglion (which give rise to unmyelinated C and Adelta fibres both conducting
nociceptive stimuli)

This is how prostaglandins produced during inflammatory states significantly increase the excitability of nociceptive nerve fibres.

So if you prevent this peripheral sensitization, hyperalgesia is reduced.
This is how NSAIDs work.
Note that NSAIDs do not affect the tenderness induced by direct application of PGs, but block the pain sensitizing mechansim induced by bradykinin, TNFalpha, interleukins (ILs) and other algesic substances.

That is why, NSAIDs are more effective against inflammation associated pain.

So now you know :)
Have a nice day


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