Abstract
Purpose: :
To investigate the effects of nepafenac, a non–steroidal antiinflammatory drug, on neural activity of corneal nociceptive fibers evoked by noxious chemical and mechanical stimulation of the cornea.
Methods: :
In anesthetized cats, single unit afferent activity was recorded from ciliary nerve filaments. Forty–nine A–delta polymodal units (mean c.v.: 6.6±0.5 m/sec) were studied. The response to mechanical stimulation with a Cochet–Bonnet esthesiometer and to pH changes elicited by 30s, 98.5%CO2 pulses applied to the corneal surface was explored. The characteristics of the impulse discharge elicited by these stimuli were compared before and at different times (1–96 min) after a single (60 µl) topical application of either 0.1% nepafenac ((NevanacTM Alcon), 0.1% diclofenac (VoltarenTM, Novartis) and 0.5% ketorolac (AcularTM, Allergan). Solutions were identified at the end of the study.
Results: :
Nepafenac was very effective in reducing the spontaneous and stimulus–evoked activity of corneal polymodal nociceptors elicited by repeated noxious stimulation with CO2 pulses, while the response of mechano–nociceptors to mechanical stimuli and of cold receptors to temperature reductions remained largely unaffected after treatment with this drug. A similar but slower and less pronounced effect on neural activity was obtained with diclofenac and ketorolac. Ongoing activity, that augmented progressively in vehicle–treated fibers, remained unchanged after diclofenac and ketorolac and was significantly reduced by nepafenac.
Conclusions: :
NSAIDs decreased impulse discharges elicited by acidic stimulation of polymodal nociceptive fibers of the cornea. Nepafenac caused a comparatively larger reduction of polymodal nociceptor activity than diclofenac and ketorolac suggesting a more pronounced analgesic effect of this drug after topical application.
Keywords: receptors: pharmacology/physiology • pharmacology