Dry eye syndrome, or keratoconjunctivitis sicca (KCS), is one of the most frequent ocular disorders. It may lead to progressive corneal opacification and blindness (1). Secretory, neuronal and mechanical processes that regulate the production and mixing of tear film constituents are functionally integrated (2). The ageing process, hormonal, environmental, iatrogenic, pharmacological and pathogenic factors may disrupt the tear film with subsequent ocular surface inflammation (3). The hyperosmolar tear film stimulates the production of mitogen-activated protein kinase (4). This initiates a cascade of protein phosphorylation involving other kinases and nuclear transcription factors which stimulate the proinflammatory cytokines and chemokines in tear fluid and conjunctival epithelium in KCS (5). The purpose of this study was to compare the topical anti-inflammatory effects of the nonselective cyclooxygenase (COX) inhibitor, ketorolac, with the selective COX-2 inhibitor, nimesulide, in an animal model of dry eye in albino rabbits. All animals were examined by the Schirmer test, tear break-up time (TBUT) and fluorescein corneal staining test. Dry eye model showed significant reduction in tear volume, TBUT, corneal staining and histopathological signs of dryness and inflammation. On treating dry eye model with nimesulide 0.1% eye drops and ketorolac 0.5% eye drops, there were improvements in Schirmer test values, TBUT and fluorescein corneal staining and histopathologically reduced inflammatory reaction, with signs of healing and regeneration. Both nimesulide and ketorolac ameliorate atropine sulphate induced dry eye in albino rabbits. The use of selective COX-2 inhibitor, nimesulide, is preferred to avoid local and systemic side effects which may occur with the use of the nonselective COX inhibitor, ketorolac.