Abstract
Purpose: :
Nitric oxide (NO) is involved in peripheral hyperalgesia control. The aim of this study was to evaluate the effect of isosorbide dinitrate (a NO donor) on corneal hyperalgesia, in a rat model of superficial silver nitrate cauterization.
Methods: :
Three groups of adult male Wistar rats (groups A, B, and C; n=6/group) were used in this study. In the groups A and B, the center of the right cornea was cauterized using a silver nitrate applicator stick (75% silver nitrate, 25% potassium nitrate) to produce a 1 mm lesion. Group C was not cauterized (control). Afterwards, topical saline (group A) and isosorbide dinitrate (200 µg/4µl, group B) were applied every 2 hours, in each treated group, respectively. Behavioral sensitization to chemical stimuli was determined, six hours later, by counting the number of blinks after one drop of 10 µM capsaicin.
Results: :
Instillation of capsaicin onto the corneal surface of non–cauterized animals (group C) induced 34.3 ± 2.0 blinks within 30 seconds. However, in cauterized animals treated with saline (group A), capsaicin induced 50.3 ± 4.6 blinks, that was statistically different of group C (P<0.01, Mann–Whitney–U test). Topical treatment of the cauterized animals with isosorbide dinitrate (group B) reduced significantly the capsaicin–induced blinks (36.2 ± 3.1 blinks; P< 0.05). There was no significantly difference between groups B and C (P=0.49).
Conclusions: :
The present data suggest that NO donors, such as isosorbide dinitrate, can reduce corneal hyperalgesia following chemical injury. Further studies using corneal cauterization models will clarify the correct pharmacological pathway underlying the ocular surface hyperalgesia.
Keywords: cornea: epithelium • inflammation • nitric oxide