Pain originating from corneal epithelial damage is a prevalent and distressing symptom caused by factors such as mechanical trauma, chemical exposure, ulceration, UV irradiation, or infection. Despite its frequency, effective and long-lasting treatments remain limited. This study evaluated a newly synthesized quaternary ammonium compound, N-propylamiodarone bromide (NPA), for its ability to provide prolonged corneal analgesia via selective entry through transient receptor potential vanilloid 1 (TRPV1) channels, while ensuring normal epithelial repair. Corneal injury was induced in 24 adult Wistar rats, which then received topical applications of saline, oxybuprocaine, or NPA (n = 8 per group). Pain responses were quantified using the von Frey filament assay. In a separate experiment, 32 rats with intact corneas were treated with oxybuprocaine, capsaicin (TRPV1 agonist), or NPA alone or in combination with capsaicin (n = 8 per group) to assess effects on mechanical sensitivity. Corneal epithelial recovery following injury and treatment was evaluated using fluorescence microscopy and hematoxylin–eosin staining in an additional 8 rats.
NPA produced markedly prolonged analgesia compared to oxybuprocaine in injured corneas (maximum effect duration: 215 ± 11 vs 25 ± 2 min, P < 0.001) without causing ocular irritation. In normal corneas, NPA did not affect baseline sensitivity; however, when co-administered with capsaicin, it induced significantly extended anesthesia relative to oxybuprocaine (165 ± 15 vs 31 ± 2 min, P < 0.001). Importantly, NPA treatment did not impede epithelial wound healing. The novel compound NPA provides durable corneal analgesia without interfering with tissue repair, representing a promising candidate for the management of pain associated with corneal injury.
