J. Gallar et al., IRRITATION OF THE ANTERIOR SEGMENT OF THE EYE BY ULTRAVIOLET-RADIATION - INFLUENCE OF NERVE BLOCKADE AND CALCIUM-ANTAGONISTS, Current eye research, 14(9), 1995, pp. 827-835
The aim of this investigation was to determine the influence on anteri
or segment inflammation elicited by UV radiation, of ocular denervatio
n and pharmacological blockade of sensory nerve fibers with capsaicin,
tetrodotoxin and calcium antagonists. Both eyes of pigmented rabbits
were exposed for 5 min to UV radiation (254 nm); 24 h later, inflammat
ory signs were evaluated by biomicroscopy of the corneal epithelium, t
he stroma and the endothelium and scored from 0 to 4. Conjunctival vas
odilation and miosis were also assessed. Two weeks before UV exposure,
a group of rabbits received a retrobulbar injection of ethanol or of
1% capsaicin. Intact, capsaicin-treated and alcohol-denervated animals
were treated topically, prior to UV exposure, with tetrodotoxin (0.78
mM) and the calcium antagonists diltiazem (1-28 mM) and nifedipine (1
0 mM). UV radiation produced at 24 h signs of corneal irritation, conj
unctival hyperemia, miosis and elevated protein content of the aqueous
humor. Retrobulbar injection of 99% alcohol or 1% capsaicin did not d
iminish significantly the inflammation of tissues directly exposed to
UV radiation, although extension of inflammatory signs to unaffected a
reas was prevented. Pre-treatment of normal and denervated eyes with d
iltiazem attenuated UV-induced eye irritation signs at concentrations
of 10 mM or over. The effect was less pronounced with tetrodotoxin and
was not obtained with nifedipine. These findings suggest that the con
tribution of a neurogenic mechanism to anterior segment inflammation i
nduced by UV exposure is modest. They also show that high concentratio
ns of diltiazem, but not of nifedipine, effectively reduced inflammati
on of the anterior segment of the eye evoked by UV radiation. This eff
ect appears to be largely independent of the blocking action of this d
rug on chemical excitation of nociceptive sensory afferents.