| Purpose:To invest the toxicity effect of benzalkonium chloride on corneal innervation.Methods:Fifty-four adult New Zealand Albino rabbits were divided into3groups randomly. Benzalkonium chloride at different concentrations of0.005%,0.01%, or0.02%was topically applied to one eye of each albino rabbit once a day, totally for9days, and the contralateral untreated eyes were served as controls. We compared aqueous tear production, Corneal mechanical sensitivity, tear break-up time (BUT), Rose Bengal and fluorescein staining scores with those of control values on days3,6,9. We examined the structure of the central cornea on day9, by measurements of in vivo confocal microscopy. whole mount corneas were immunostained with anti-tubulin βⅢ antibody, a specific antibody labeling nerve fibers. The presence of anti-tubulin βⅢ was analyzed by means of fluorescence confocal microscopy, and nerve fiber densities of stromal nerve, subbasal nerve, and epithelial superficial nerve terminal were quantified.Results:The BAK-treated eyes exhibited a lower corneal sensitivity on day3, and increased the score of Rose Bengal staining, no significant changes were found in the corneal fluorescein scores, BUT, and Schirmer scores. The topical application of BAK induced a lower nerve densities in superficial and subbasal layers on days3and6. BUT, Schirmer scores, and stromal nerve fiber density were significantly reduced in eyes treated with0.02%BAK, and fluorescein staining scores increased on day9. Corneal superficial epithelial cell size in all BAK-treated eyes was significantly larger than that in control eyes.Conclusions:Exposure to benzalkonium chloride can change the corneal innervation. It quickly induce corneal hypoesthesia without reducing the tear secretion. Changes in corneal innervation significantly correlate with BAK-induced ocular surface changes. |